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Journal articles on the topic 'Vinclozolin'

Author: Grafiati

Published: 4 June 2021

Last updated: 10 March 2023

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1

Di Paola, Davide, Ramona D’Amico, Tiziana Genovese, Rosalba Siracusa, Marika Cordaro, Rosalia Crupi, Alessio Filippo Peritore, et al. "Chronic Exposure to Vinclozolin Induced Fibrosis, Mitochondrial Dysfunction, Oxidative Stress, and Apoptosis in Mice Kidney." International Journal of Molecular Sciences 23, no. 19 (September 25, 2022): 11296. http://dx.doi.org/10.3390/ijms231911296.

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Vinclozolin is one of the most used fungicides in the control of fungi in fruits, vegetables, and ornamental plants. The effects of its exposure on different organs have been described, but information regarding its relevance to vinclozolin-induced nephrotoxicity is largely missing. This study focuses on the potential mechanism of vinclozolin-induced nephrotoxicity. CD1 male mice were administered vinclozolin (100 mg/kg) by oral gavage for 28 days. Vinclozolin administration decreased body weight over the treatment period and at the end of the experiment, increased the ratio of kidney weight to body weight and increased serum urea nitrogen and creatinine contents. Vinclozolin also induced histopathological alterations, including tubular dilatation and necrosis and impaired the integrity of the renal-tubular architecture and kidney fibrosis. The analyses conducted showed that vinclozolin administration altered the mRNA levels of mitochondrial function-related proteins (SIRT3, SIRT1, PGC-1α, TFAM, NRF1, VDAC-1, and Cyt c) and oxidative stress (increased lipid peroxidation and decreased total antioxidative capacity, catalase, and superoxide dismutase activities, glutathione levels, and glutathione peroxidase activity) in the kidneys. Furthermore, vinclozolin induced toxicity that altered Nrf2 signalling and the related proteins (HO-1 and NQO-1). Vinclozolin administration also affected both the extrinsic and intrinsic apoptotic pathways, upregulating the expression of proapoptotic factors (Bax, Caspase 3, and FasL) and downregulating antiapoptotic factor (Bcl-2) levels. This study suggests that vinclozolin induced nephrotoxicity by disrupting the transcription of mitochondrial function-related factors, the Nrf2 signalling pathway, and the extrinsic and intrinsic apoptotic pathways.

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2

Cabral, Silvia M. J. C. S., and João P. S. Cabral. "Morphological and chemical alterations inBotrytis cinereaexposed to the dicarboximide fungicide vinclozolin." Canadian Journal of Microbiology 43, no. 6 (June 1, 1997): 552–60. http://dx.doi.org/10.1139/m97-078.

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Treatment of actively growing Botrytis cinerea hyphae with micromolar concentrations of the dicarboximide fungicide vinclozolin resulted in significant alterations in the growth rate, morphology, and chemical composition of the cells. The addition of vinclozolin resulted in an immediate and severe reduction in the hyphal growth rate and a retardation in the emergence of the second germ tube. Cells treated with vinclozolin had a lower content of pool metabolites than control cells, and this difference increased with time of exposure to the fungicide. In contrast, vinclozolin-treated cells had a higher chitin concentration than control cells. These biochemical alterations were followed by the disorganization and clearing of cells, and by the appearance of dense and dark masses outside the hyphae, presumably composed of cell debris. Hyphae exposed to vinclozolin were more curved and branched and had shorter cells than the controls. The results indicate that vinclozolin causes a slow but generalized leakage of pool metabolites; this release precedes cell lysis and is not the result of a rapid and gross damage to the cytoplasmic membrane.Key words: vinclozolin, Botrytis cinerea, pool metabolites, membrane damage.

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3

Cowin, Prue A., Elspeth Gold, Jasna Aleksova, Moira K. O'Bryan, Paul M. D. Foster, Hamish S. Scott, and Gail P. Risbridger. "Vinclozolin Exposure in Utero Induces Postpubertal Prostatitis and Reduces Sperm Production via a Reversible Hormone-Regulated Mechanism." Endocrinology 151, no. 2 (February 1, 2010): 783–92. http://dx.doi.org/10.1210/en.2009-0982.

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Vinclozolin is an endocrine-disrupting chemical (EDC) that binds with high affinity to the androgen receptor (AR) and blocks the action of gonadal hormones on male reproductive organs. An alternative mechanism of action of Vinclozolin involves transgenerational effects on the male reproductive tract. We previously reported in utero Vinclozolin exposure-induced prostatitis (prostate inflammation) in postpubertal rats concurrent with down-regulation of AR and increased nuclear factor-κB activation. We postulated the male reproductive abnormalities induced by in utero Vinclozolin exposure could be reversed by testosterone supplementation, in contrast to the permanent modifications involving DNA methyltransferases (Dnmts) described by others. To test this hypothesis, we administered high-dose testosterone at puberty to Vinclozolin-treated rats and determined the effect on anogenital distance (AGD); testicular germ cell apoptosis, concentration of elongated spermatids, and the onset of prostatitis. Concurrently we examined Dnmt1, −3A, −3B, and −3L mRNA expression. Consistent with previous reports, in utero exposure to Vinclozolin significantly reduced AGD, increased testicular germ cell apoptosis 3-fold, reduced elongated spermatid number by 40%, and induced postpubertal prostatitis in 100% of exposed males. Administration of high-dose testosterone (25 mg/kg) at puberty normalized AGD, reduced germ cell apoptosis, and restored elongated spermatid number. Testosterone restored AR and nuclear factor-κB expression in the prostate and abolished Vinclozolin-induced prostatitis. Altered Dnmt expression was evident with in utero Vinclozolin exposure and was not normalized after testosterone treatment. These data demonstrate in utero Vinclozolin-induced male reproductive tract abnormalities are AR mediated and reversible and involve a mechanism independent of Dnmt expression.

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4

D’Amico, Ramona, Davide Di Paola, Daniela Impellizzeri, Tiziana Genovese, Roberta Fusco, Alessio Filippo Peritore, Enrico Gugliandolo, et al. "Chronic Exposure to Endocrine Disruptor Vinclozolin Leads to Lung Damage Via Nrf2–Nf-kb Pathway Alterations." International Journal of Molecular Sciences 23, no. 19 (September 26, 2022): 11320. http://dx.doi.org/10.3390/ijms231911320.

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Endocrine-disrupting substances (EDS) are common and pervasive in our environment and pose a serious risk to both human and animal health. Endocrine-disrupting compounds (EDCs) have been associated with a variety of detrimental human health effects, including respiratory issues, as a result of their ability to disrupt cell physiology. Vinclozolin ((RS)-3-(3,5-Dichlorophenyl)-5-methyl-5-vinyloxazolidine-2,4-dione) is a common dicarboximide fungicide used to treat plant diseases. Several studies have analyzed the effects of vinclozolin exposure on the reproductive system, but less is known about its effect on other organs such as the lung. Mice were exposed for 28 days to orally administered vinclozolin at a dose of 100 mg/kg. Vinclozolin exposure induced histological alterations and collagen depositions in the lung. Additionally, vinclozolin induced inflammation and oxidative stress that led to lung apoptosis. Our study demonstrates for the first time that the toxicological effects of vinclozolin are not limited to the reproductive system but also involve other organs such as the lung.

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5

Veeramachaneni, D. N. R., J. S. Palmer, R. P. Amann, C. M. Kane, T. T. Higuchi, and K.-Y. F. Pau. "Disruption of sexual function, FSH secretion, and spermiogenesis in rabbits following developmental exposure to vinclozolin, a fungicide." Reproduction 131, no. 4 (April 2006): 805–16. http://dx.doi.org/10.1530/rep.1.01048.

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We studied sequelae of prenatal plus infantile exposure of male rabbits to vinclozolin, because it is ingested by women and children. Female Dutch-Belted rabbits (7–10/group) were treated daily per orum from gestation day 15 through post-natal week 4 to provide 0, 7.2, or 72 mg vinclozolin/kg dam’s body weight/day. Vinclozolin had no effect on maintenance of pregnancy, growth of pups, age at testicular descent or weight of organs. Concentrations of serum LH or testosterone at 6, 12, or 24 weeks of age were unaffected. However, FSH was lower (P< 0.05) in both vinclozolin groups at all three ages. Following injection of GnRH at 12 or 24 weeks, the increase in FSH was less (P< 0.05) in both vinclozolin groups, as was testosterone at 12 weeks of age. After full sexual maturity, 2 of 7 low dose rabbits were uninterested in female or male teasers and never achieved erection or ejaculation. Overall, rates of ejaculation failure were: control 0% (0/48), low dose 29% (12/42), and high dose 5% (3/60). Daily sperm production per gram of testis and total number of sperm per ejaculate in both vinclozolin groups were similar (P> 0.1) to controls. However, semen from vinclozolin rabbits contained over two times more (P< 0.05) morphologically abnormal spermatozoa, mostly nuclear and acrosomal defects, than semen from controls. Seminiferous tubules with degenerative changes were more frequent (P< 0.05) in vinclozolin rabbits than in controls. Lesions included syncytia of spherical spermatids and desquamation of germ cells. Hence, developmental exposure to vinclozolin caused presumably permanent changes in copulatory ability, secretion of FSH, and spermiogenesis.

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6

Shen, Xiuwei, Fan Chen, Lanlan Chen, Ying Su, Ping Huang, and Ren-Shan Ge. "Effects of Fungicides on Rat’s Neurosteroid Synthetic Enzymes." BioMed Research International 2017 (2017): 1–8. http://dx.doi.org/10.1155/2017/5829756.

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Exposure to environmental endocrine disruptors may interfere with nervous system’s activity. Fungicides such as tebuconazole, triadimefon, and vinclozolin have antifungal activities and are used to prevent fungal infections in agricultural plants. In the present study, we studied effects of tebuconazole, triadimefon, and vinclozolin on rat’s neurosteroidogenic 5α-reductase 1 (5α-Red1), 3α-hydroxysteroid dehydrogenase (3α-HSD), and retinol dehydrogenase 2 (RDH2). Rat’s 5α-Red1, 3α-HSD, and RDH2 were cloned and expressed in COS-1 cells, and effects of these fungicides on them were measured. Tebuconazole and triadimefon competitively inhibited 5α-Red1, with IC50 values of 8.670 ± 0.771 × 10−6 M and 17.390 ± 0.079 × 10−6 M, respectively, while vinclozolin did not inhibit the enzyme at 100 × 10−6 M. Triadimefon competitively inhibited 3α-HSD, with IC50 value of 26.493 ± 0.076 × 10−6 M. Tebuconazole and vinclozolin weakly inhibited 3α-HSD, with IC50 values about 100 × 10−6 M, while vinclozolin did not inhibit the enzyme even at 100 × 10−6 M. Tebuconazole and triadimefon weakly inhibited RDH2 with IC50 values over 100 × 10−6 M and vinclozolin did not inhibit this enzyme at 100 × 10−6 M. Docking study showed that tebuconazole, triadimefon, and vinclozolin bound to the steroid-binding pocket of 3α-HSD. In conclusion, triadimefon potently inhibited rat’s neurosteroidogenic enzymes, 5α-Red1 and 3α-HSD.

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7

Nilsson, Eric E., Matthew D. Anway, Jacob Stanfield, and Michael K. Skinner. "Transgenerational epigenetic effects of the endocrine disruptor vinclozolin on pregnancies and female adult onset disease." REPRODUCTION 135, no. 5 (May 2008): 713–21. http://dx.doi.org/10.1530/rep-07-0542.

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Endocrine disruptor exposure during gonadal sex determination was previously found to induce male rat adult onset transgenerational disease (F1–F4 generation), and this was associated with an alteration in the epigenetic (i.e., DNA methylation) programming of the male germ line. The current study was designed to characterize the transgenerational disease phenotypes of the female adult offspring. Pregnant rats (F0 generation) were treated transiently with vinclozolin (i.e., fungicide with anti-androgenic activity) on embryonic (E) days E8–E14 of gestation. F1 control and vinclozolin generation offspring from different litters were mated to produce F2 offspring, and similarly F2 generation animals produced F3 generation offspring. Observations demonstrated that 9 out of 105 pregnant rats (8.6%) from the vinclozolin F1–F3 generations exhibited uterine hemorrhage and/or anemia late in pregnancy. None (0 out of 82) of the control F1–F3 generation females had similar pregnancy problems. Complete blood cell counts and serum chemistry profiles demonstrated that selected vinclozolin generation animals, but not controls, exhibited marked regenerative anemia in late pregnancy. Examination of kidney histology revealed moderate or severe glomerular abnormalities in 67% of the vinclozolin F2 and F3 generation adult females compared with 18% of the controls. Adult female vinclozolin generation animals also developed various types of tumors in 6.5% of the animals (11 out of 170), while 2% of control-line animals (3 out of 151) developed mammary tumors. Observations demonstrate that vinclozolin exposure during gonadal sex determination promotes a transgenerational increase in pregnancy abnormalities and female adult onset disease states.

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8

Matheron, M. E., and M. Porchas. "Activity of Boscalid, Fenhexamid, Fluazinam, Fludioxonil, and Vinclozolin on Growth of Sclerotinia minor and S. sclerotiorum and Development of Lettuce Drop." Plant Disease 88, no. 6 (June 2004): 665–68. http://dx.doi.org/10.1094/pdis.2004.88.6.665.

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Sclerotinia drop is a major disease of lettuce caused by two soilborne fungi, Sclerotinia minor and S. sclerotiorum. Fungicides such as dicloran (Botran), iprodione (Rovral), and vinclozolin (Ronilan) are currently available in the United States to manage this disease. Studies were conducted to investigate the relative effect of some new fungicides, including boscalid, fenhexamid, fluazinam, and fludioxonil, in comparison with vinclozolin, on growth of S. minor and S. sclerotiorum in agar plate tests as well as control of lettuce drop in the field. At a rate of 0.001 μg/ml, all tested compounds only suppressed mycelial growth of either pathogen from 0 to 20%. At 0.01 μg/ml, mycelial growth of S. minor was reduced 82 to 84% by fludioxonil and fluazinam and only 1 to 16% by boscalid, fenhexamid, and vinclozolin. At the same rate, mycelial growth of S. sclerotiorum was reduced 78% by fluazinam and from 0 to 12% by boscalid, fludioxonil, fenhexamid, and vinclozolin. At 0.1 μg/ml, all tested chemistries except vinclozolin inhibited mycelial growth of S. minor from 70 to 98%, whereas growth of S. sclerotiorum was suppressed 95 to 99% by fludioxonil and fluazinam, significantly less (40 to 47%) by boscalid and fenhexamid, and not at all by vinclozolin. At a rate of 1.0 μg/ml, all tested fungicides reduced mycelial growth of S. minor and S. sclerotiorum from 87 to 100% and 77 to 100%, respectively. Mycelial growth emerging from sclerotia of S. minor was reduced from 98 to 100% by all fungicides tested at a rate of 1.0 μg/ml, whereas growth from sclerotia of S. sclerotiorum was suppressed from 90 to 96% by fenhexamid, fludioxonil, fluazinam, and vinclozolin. In lettuce plots infested with S. minor, boscalid and fluazinam provided the highest level of disease control, significantly greater than that achieved with fenhexamid, fludioxonil, and vinclozolin. In the presence of S. sclerotiorum, the highest degree of disease suppression occurred with application of fluazinam, fludioxonil, and vinclozolin, whereas the least effective compound was fenhexamid. Boscalid and fluazinam were more effective against lettuce drop caused by S. minor than disease caused by S. sclerotiorum.

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9

Yourman, L. F., and S. N. Jeffers. "Resistance to Benzimidazole and Dicarboximide Fungicides in Greenhouse Isolates of Botrytis cinerea." Plant Disease 83, no. 6 (June 1999): 569–75. http://dx.doi.org/10.1094/pdis.1999.83.6.569.

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In 1996 and 1997, 325 isolates of Botrytis cinerea were collected from 35 commercial greenhouses growing ornamental crops in South Carolina to determine the incidence of resistance to benzimidazole and dicarboximide fungicides. Conidium germination was assessed on a defined agar medium amended with either thiophanate-methyl (a benzimidazole) or vinclozolin (a di-carboximide). A total of 53 representative isolates were evaluated further for conidium germination and mycelium growth on fungicide-amended medium and for infection of geranium seedlings treated with thiophanate-methyl or vinclozolin at label rates. Isolates were considered sensitive to thiophanate-methyl or vinclozolin when the effective concentration of the fungicide active ingredient resulting in 50% inhibition of germination (EC50-germ) was ≤5 μg/ml or when the effective concentration of fungicide active ingredient resulting in 50% inhibition of mycelium growth (EC50-growth) was ≤1 μg/ml. Of all isolates, 81% (262/325) were resistant to thiophanate-methyl and 69% (223/325) were resistant to vinclozolin. Four phenotypes were observed: sensitive to both fungicides (17%), resistant to both fungicides (67%), resistant only to thiophanate-methyl (14%), and resistant only to vinclozolin (2%). Isolates resistant to at least one fungicide were found in 33 of the 35 locations from which samples were taken. Disease incidences on geranium seedlings treated with 600 μg/ml of thiophanate-methyl and then inoculated with isolates sensitive and resistant to this fungicide were 1.4 and 96.1%, respectively. Disease incidences on geranium seedlings treated with 600 μg/ml of vinclozolin and then inoculated with isolates sensitive and resistant to this fungicide were 0.3 and 91.9%, respectively. With thiophanate-methyl, correlation coefficients (r) between disease incidence and log EC50-germ or log EC50-growth were 0.987 and 0.992, respectively. With vinclozolin, correlation coefficients between disease incidence and log EC50-germ and log EC50-growth were 0.975 and 0.893, respectively. Correlation coefficients between the two EC50 values for thiophanate-methyl were 0.989 and for vinclozolin were 0.900. Isolates sensitive to thiophanate-methyl had a mean EC50-germ value of 0.93 μg/ml and a EC50-growth value of 0.11 μg/ml. For isolates sensitive to vinclozolin the mean EC50-germ value was 1.63 μg/ml and the mean EC50-growth value was 0.26 μg/ml. Thiophanate-methyl-resistant isolates had mean EC50-germ and EC50-growth values greater than 500 μg/ml while vinclozolin-resistant isolates had a mean EC50-germ value greater than 500 μg/ml and a mean EC50-growth value of 3.18 μg/ml.

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10

Tanovic, Brankica, Jovana Hrustic, Mila Grahovac, Milica Mihajlovic, Goran Delibasic, and Petar Vuksa. "Is low efficacy of fungicides always a consequence of fungicide resistance development in pathogen populations?" Pesticidi i fitomedicina 26, no. 4 (2011): 347–54. http://dx.doi.org/10.2298/pif1104347t.

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Efficacy of four fungicides with different modes of action (vinclozolin, pyrimethanil, benomyl and fenhexamid) in control of B. cinerea in raspberry, was investigated in the paper. The trials were conducted at two localities in commercial raspberry plantations. In the case of unsatisfactory fungicide efficacy, qualitative and/or quantitative test of the susceptibility of the isolates to particular fungicide was performed, to determine whether the low efficacy is a consequence of resistance development in the pathogen population. At both localities, pyrimethanil and fenhexamid demonstrated the highest efficacy (73.2-89.6%), while the efficacy of vinclozolin was statistically significantly lower (48.7-63.4%) at both localities. However, qualitative and quantitative test of susceptibility to vinclozolin showed that all the isolates were susceptible to vinclozolin and that the reason for unsatisfactory efficacy should be primarily sought in inadequate fungicide application.

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11

Porter, D. M., and P. M. Phipps. "Tolerance of Sclerotinia minor to Procymidone and Cross Tolerance to Other Dicarboximide Fungicides and Dicloran1." Peanut Science 12, no. 1 (January 1, 1985): 41–45. http://dx.doi.org/10.3146/pnut.12.1.0010.

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Abstract Procymidone-tolerant isolates of Sclerotinia minor Jagger were cross-tolerant to iprodione, vinclozolin and dicloran. Hyphal growth of procymidone-tolerant isolates an agar amended with 1 to 100 μg/mL procymidone, iprodione, vinclozolin or dicloran was similar. Procymidone-tolerant isolates were tolerant to all fungicides after 10 weekly hyphal tip transfers to nonamended agar. Subsequently, cross-tolerance persisted on agar amended with either 10 μg/mL procymidone, iprodione, vinclozolin or dicloran. Most procymidone-tolerant isolates of S. minor were pathogenic to peanuts (Arachis hypogaea L.) and caused symptoms similar to those initiated by sensitive isolates.

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12

Buck, J. W., and S. N. Jeffers. "Effect of Pathogen Aggressiveness and Vinclozolin on Efficacy of Rhodotorula glutinis PM4 Against Botrytis cinerea on Geranium Leaf Disks and Seedlings." Plant Disease 88, no. 11 (November 2004): 1262–68. http://dx.doi.org/10.1094/pdis.2004.88.11.1262.

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Efficacy of the yeast Rhodotorula glutinis isolate PM4 as a biological control agent against 29 isolates of Botrytis cinerea obtained from greenhouse-grown ornamentals was assessed in vitro on geranium leaf disks. Isolates of B. cinerea varied in aggressiveness in the absence of either biological or chemical controls; diameters of lesions produced on leaf disks ranged from 0.8 to 12.3 mm. Efficacy of R. glutinis PM4 against the different isolates of B. cinerea varied greatly; lesion diameters ranged from 0.2 to 10.3 mm when the yeast was present. The yeast significantly reduced lesion development by 16 B. cinerea isolates in each of two replicate trials and by 9 isolates in one of the trials; however, 3 isolates were not inhibited by the yeast on geranium leaf disks. The yeast significantly reduced lesion development by B. cinerea isolate 01, used as a standard for comparison, in four of six trials. Fourteen of the B. cinerea isolates were inoculated onto geranium seedlings and produced a range of lesion sizes (2.9 to 16.4 mm), similar to that produced on leaf disks. Efficacy of the yeast in combination with a reduced rate (0.1×) of the fungicide vinclozolin (50 μg of active ingredient ml-1) was evaluated on geranium seedlings against 10 isolates of B. cinerea that were resistant to vinclozolin. Addition of vinclozolin to the yeast significantly reduced lesion diameter by five of the isolates compared with diameters of lesions produced in the presence of the yeast alone. Lesions produced by nine of the resistant isolates were 2.6 mm or smaller in both trials on plants treated with the mixture of yeast and vinclozolin. The effect of vinclozolin concentration (0 to 500 μg a.i. ml-1) on biocontrol efficacy of R. glutinis PM4 was evaluated using three resistant isolates of B. cinerea and geranium seedlings. Disease control was significantly better at higher concentrations of fungicide for two of the isolates. Linear regression of lesion diameter against vinclozolin concentration showed a significant effect on yeast biocontrol efficacy with B. cinerea isolate FL-2-b (y = 6.20 – 0.63x; r2= 0.74) and isolate BR-1 (y = 4.10 – 0.32x; r2 =0.28) but there was no significant effect with isolate GG-2-b. Overall, PM4 exhibited biocontrol activity on both geranium leaf disks and seedlings against a number of isolates of B. cinerea that varied in aggressiveness. Variability in biocontrol efficacy against isolates resistant to vinclozolin usually was reduced by the addition of vinclozolin.

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13

Li, G. Q., H. C. Huang, and S. N. Acharya. "Sensitivity of Ulocladium atrum, Coniothyrium minitans, and Sclerotinia sclerotiorum to benomyl and vinclozolin." Canadian Journal of Botany 80, no. 8 (August 1, 2002): 892–98. http://dx.doi.org/10.1139/b02-077.

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Assays on mycelial growth and spore germination were carried out to determine the sensitivity of the biocontrol agents Ulocladium atrum and Coniothyrium minitans and the plant pathogen Sclerotinia sclerotiorum to benomyl and vinclozolin. Ulocladium atrum was more tolerant to these fungicides than C. minitans and S. sclerotiorum. The 50% effective concentration (EC50) of U. atrum based on the mycelial growth inhibition was 1467.3 µg active ingredient (a.i.)/mL for benomyl and 12.6 µg a.i./mL for vinclozolin, and the maximum inhibition concentration was higher than 4000 µg a.i./mL for both fungicides. For C. minitans and S. sclerotiorum, however, the EC50 based on mycelial growth inhibition was lower than 1 µg a.i./mL. After incubation for 24 h at 20°C, the germination rate of U. atrum conidia was 9099% on potato dextrose agar (PDA) amended with benomyl at 100500 µg a.i./mL or vinclozolin at 10500 µg a.i./mL. At these concentrations, germ tubes of U. atrum developed into long, branched hyphae in benomyl treatments, but they remained short and clustered in vinclozolin treatments. Pycnidiospores of C. minitans and ascospores of S. sclerotiorum germinated on PDA amended with benomyl at 100500 µg a.i./mL, but the germ tubes did not grow further. Spore germination of C. minitans and S. sclerotiorum was less than 3.2% on PDA amended with vinclozolin at 10500 µg a.i./mL after 24 h. This is the first report on the sensitivity of U. atrum and C. minitans to benomyl and vinclozolin. The results suggest that it is possible to control S. sclerotiorum using a combination of U. atrum and benomyl or vinclozolin.Key words: fungicides, mycelial growth, spore germination, integrated pest management.

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Yourman, L. F., S. N. Jeffers, and R. A. Dean. "Genetic Analysis of Isolates of Botrytis cinerea Sensitive and Resistant to Benzimidazole and Dicarboximide Fungicides." Phytopathology® 90, no. 8 (August 2000): 851–59. http://dx.doi.org/10.1094/phyto.2000.90.8.851.

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A total of 56 isolates of B. cinerea collected from ornamental crops from commercial greenhouses were examined by random amplified polymorphic DNA (RAPD) fingerprint analyses. Isolates were examined as two independent sets of 35 and 36 isolates, with 15 isolates common to both sets. The isolates had four phenotypes: 17 were sensitive to two commonly used fungicides, thiophanate-methyl (a benzimidazole) and vinclozolin (a dicarboximide) (STSV); 18 were resistant to both fungicides (RTRV); 16 were resistant to thiophanate-methyl but sensitive to vinclozolin (RTSV); and 5 were sensitive to thiophanate-methyl but resistant to vinclozolin (STRV). Relationships among the isolates were determined by cluster analyses of mean character differences using the unweighted pair group method using arithmetic average and cladograms were constructed. Isolates were clustered primarily by fungicide-sensitivity phenotype. In one set of greenhouse isolates, 6 of 10 STSV isolates clustered together with a bootstrap confidence value of 91%. In the other fingerprint set of greenhouse isolates, 9 of 11 STSV isolates clustered together and had a bootstrap confidence value of 98%. Isolates resistant to thiophanate-methyl, vinclozolin, or both fungicides usually were not clustered with other isolates or were clustered with isolates of the same phenotype. To further elucidate these relationships, variant isolates resistant to one or both fungicides were produced on fungicide-amended agar medium from 14 STSV greenhouse isolates. These 14 STSV parent isolates, 57 resistant variant isolates, and 11 resistant greenhouse isolates were analyzed as three independent RAPD fingerprint sets. Variants selected from eight STSV parent isolates were resistant to both thiophanate-methyl and vinclozolin even though parent isolates were exposed to only one of the fungicides. Isolates resistant only to vinclozolin (STRV) had fingerprint patterns similar to and clustered with those of parent isolates, while fingerprint patterns of isolates resistant to thiophanate-methyl (i.e., RTRV or RTSV), regardless of sensitivity to vinclozolin, clustered differently from both those of STSV parent isolates and those of STRV isolates derived from the same parent. RTRV and RTSV variant isolates derived from the same fungicide-sensitive parents only clustered with other variants having the same phenotype.

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15

Zhou, Ting, and R. D. Reeleder. "Selection of strains of Epicoccum purpurascens for tolerance to fungicides and improved biocontrol of Sclerotinia sclerotiorum." Canadian Journal of Microbiology 36, no. 11 (November 1, 1990): 754–59. http://dx.doi.org/10.1139/m90-130.

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A wild-type isolate of Epicoccum purpurascens was exposed to shortwave ultraviolet light. One of the resulting cultures (M-20-A) was grown on media amended with the fungicides iprodione or vinclozolin and fungicide-tolerant strains were obtained. Several comparisons were made between new strains and the wild type. Sporulation was improved compared with the wild type. Strains varied in their tolerance to iprodione and vinclozolin but were not tolerant to the fungicide benomyl. Strains R4000, 16-B, and 7-A inhibited Sclerotinia sclerotiorum in vitro more than either the wild type or M-20-A, and exhibited improved control of white mold of bean in the greenhouse compared with M-20-A. Key words: biological control, fungicide resistance, white mold, iprodione, vinclozolin.

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16

Buck, J. W. "Combinations of Fungicides with Phylloplane Yeasts for Improved Control of Botrytis cinerea on Geranium Seedlings." Phytopathology® 94, no. 2 (February 2004): 196–202. http://dx.doi.org/10.1094/phyto.2004.94.2.196.

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Control of Botrytis cinerea on geranium seedlings was evaluated in treatments with phylloplane yeasts in combination with 10 fungicides used to manage Botrytis blight of ornamental plants. Rhodotorula glutinis PM4 significantly reduced the development of lesions caused by B. cinerea on geranium cotyledons; however, yeast biocontrol efficacy was highly variable between trials. Treatment with the yeast in combination with azoxystrobin or trifloxystrobin at one tenth the labeled rate (7.5 μg a.i. ml-1) or the full labeled rate (7.5 μg a.i. ml-1) reduced lesion development, compared to treatment with the yeast or the fungicide alone. Vinclozolin at half the labeled rate or the full labeled rate (250 or 500 μg a.i. ml-1), in combination with R. glutinis PM4, significantly reduced the development of lesions caused by an isolate of B. cinerea resistant to vinclozolin. Copper hydroxide and iprodione at one-tenth the labeled rates, with or without yeast, were highly effective in limiting lesion development. Mancozeb did not increase the biocontrol efficacy of the yeast, and thiophanate-methyl negatively affected the yeast efficacy. Improved disease control was observed in treatments with vinclozolin at the labeled rate and R. glutinis PM4 at cell densities of 5 × 105 and 1 × 106 cells ml-1, but not 1 × 105 cells ml-1, on seedlings co-inoculated with B. cinerea in a suspension containing 1 × 105 conidia ml-1. Disease control improved in treatments with combinations of vinclozolin and eight other isolates of R. glutinis, two isolates of R. graminis, and two isolates of R. mucilaginosa. Biocontrol was not observed in treatments with two isolates of R. minuta. The combination of yeast and vinclozolin significantly reduced the germination of conidia of B. cinerea and the growth of R. glutinis PM4 in vitro. All combinations of R. glutinis PM4 with azoxystrobin, trifloxystrobin, or vinclozolin provided highly effective and consistent disease control not observed in treatments with the fungicides alone or the yeast alone.

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Golovleva, L. A., Z. I. Finkelstein, A. V. Polyakova, B. P. Baskunov, and M. Yu Nefedova. "Microbial conversion of fungicide vinclozolin." Journal of Environmental Science and Health, Part B 26, no. 3 (June 1991): 293–307. http://dx.doi.org/10.1080/03601239109372736.

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Koçkaya, Evrim Arzu, Aysun Kılıç Süloğlu, Elif Karacaoğlu, and Güldeniz Selmanoğlu. "Vinclozolin exposure throughout pregnancy and its developmental toxicity." Toxicol. Res. 3, no. 5 (2014): 375–83. http://dx.doi.org/10.1039/c4tx00037d.

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19

Tremblay, D. M., B. G. Talbot, and O. Carisse. "Sensitivity of Botrytis squamosa to Different Classes of Fungicides." Plant Disease 87, no. 5 (May 2003): 573–78. http://dx.doi.org/10.1094/pdis.2003.87.5.573.

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An automated quantitative (AQ) assay was compared with radial growth on solid media and with dry weight in liquid culture for assaying fungicide sensitivity in Botrytis squamosa, the causal agent of onion leaf blight. Five isolates of B. squamosa were assayed for sensitivity to mancozeb (Dithane DG) and iprodione (Rovral) at five concentrations (0.5, 1.0, 5.0, 10.0, and 50 ppm). For mancozeb, the correlations between 50% effective concentration (EC50) values obtained with the three assays were not significant; however for iprodione, correlations between EC50 values for AQ and radial growth and for AQ and dry weight were significant (r = 0.98 and 0.99, respectively). The AQ method was less time consuming and more reliable than the two standard assays. The AQ method was used to evaluate the sensitivity of 35 field isolates of B. squamosa to mancozeb (Dithane DG), iprodione (Rovral), vinclozolin (Ronilan DF), and chlorothalonil (Bravo 500). All isolates were sensitive to mancozeb (EC50 ranged from 3.36 to 12.97) and chlorothalonil (EC50 < 1.5 μg/ml), but four isolates were insensitive to both iprodione (EC50 ≥ 3.98 μg/ml) and vinclozolin (EC50 ≥ 17.49 μg/ml). The ratio of the EC50 values of the least-sensitive and the most-sensitive isolates of B. squamosa was 1.08, 3.86, 6.98, and 37.59 for chlorothalonil, mancozeb, iprodione, and vinclozolin, respectively. Cross-resistance was observed for the two dicarboximide fungicides, iprodione and vinclozolin, with a significant correlation (r = 0.94) in the sensitivity of the 35 isolates to these two fungicides.

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20

Chang, Hung-Shu, Matthew D. Anway, Stephen S. Rekow, and Michael K. Skinner. "Transgenerational Epigenetic Imprinting of the Male Germline by Endocrine Disruptor Exposure during Gonadal Sex Determination." Endocrinology 147, no. 12 (December 1, 2006): 5524–41. http://dx.doi.org/10.1210/en.2006-0987.

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Embryonic exposure to the endocrine disruptor vinclozolin at the time of gonadal sex determination was previously found to promote transgenerational disease states. The actions of vinclozolin appear to be due to epigenetic alterations in the male germline that are transmitted to subsequent generations. Analysis of the transgenerational epigenetic effects on the male germline (i.e. sperm) identified 25 candidate DNA sequences with altered methylation patterns in the vinclozolin generation sperm. These sequences were identified and mapped to specific genes and noncoding DNA regions. Bisulfite sequencing was used to confirm the altered methylation pattern of 15 of the candidate DNA sequences. Alterations in the epigenetic pattern (i.e. methylation) of these genes/DNA sequences were found in the F2 and F3 generation germline. Therefore, the reprogramming of the male germline involves the induction of new imprinted-like genes/DNA sequences that acquire an apparent permanent DNA methylation pattern that is passed at least through the paternal allele. The expression pattern of several of the genes during embryonic development were found to be altered in the vinclozolin F1 and F2 generation testis. A number of the imprinted-like genes/DNA sequences identified are associated with epigenetic linked diseases. In summary, an endocrine disruptor exposure during embryonic gonadal sex determination was found to promote an alteration in the epigenetic (i.e. induction of imprinted-like genes/DNA sequences) programming of the male germline, and this is associated with the development of transgenerational disease states.

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21

Wicks, T., and B. Philp. "Effects of iprodione and vinclozolin seed treatments on germination, emergence and plant growth in onion." Australian Journal of Experimental Agriculture 25, no. 2 (1985): 465. http://dx.doi.org/10.1071/ea9850465.

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Iprodione or vinclozolin dusted on White Spanish and Goldberg onions, at 100g a.i./kg of seed, reduced germination by at least 40% and severely stunted the growth of seedlings nated on moistened filter paper. Similar rates of vinclozolin severely reduced field emergence and retarded the growth of White Spanish and Goldberg seedlings whereas the same rate of iprodione reduced field emergence and growth of Goldberg, but not White Spanish. Poor field emergence of treated seed could have been a germi consequence of inhibition of germination, stunted seedling growth or a combination of both factors.

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22

Mueller, D. S., A. E. Dorrance, R. C. Derksen, E. Ozkan, J. E. Kurle, C. R. Grau, J. M. Gaska, G. L. Hartman, C. A. Bradley, and W. L. Pedersen. "Efficacy of Fungicides on Sclerotinia sclerotiorum and Their Potential for Control of Sclerotinia Stem Rot on Soybean." Plant Disease 86, no. 1 (January 2002): 26–31. http://dx.doi.org/10.1094/pdis.2002.86.1.26.

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Sclerotinia stem rot of soybean, caused by Sclerotinia sclerotiorum, is a major disease in the north central region of the United States. One approach to managing Sclerotinia stem rot on soybean is the use of fungicides. S. sclerotiorum was assayed for sensitivity to benomyl, tebuconazole, thiophanate methyl, and vinclozolin in pure cultures on agar medium, inoculated soybean seedlings, detached inoculated leaves, and in experimental field plots. To evaluate the inhibitory effect of four fungicides on growth of S. sclerotiorum in vitro, potato dextrose agar (PDA) was amended with the fungicides at six concentrations. Based on measurements of fungal radial growth, vinclozolin was the most effective in inhibiting S. sclerotiorum mycelial growth at 1.0 μg a.i./ml of PDA. Ranges of reduction of radial growth of 91 isolates of S. sclerotiorum on PDA amended with thiophanate methyl and vinclozolin were 18 to 93% and 93 to 99%, respectively, when compared with the nonamended agar control. Benomyl, thiophanate methyl, and vinclozolin applied to greenhouse-grown seedlings prevented S. sclerotiorum from expressing symptoms or signs on leaf tissue. Detached leaves sprayed with thiophanate methyl and then inoculated with mycelial plugs of S. sclerotiorum did not express symptoms or signs. Of 13 different environments in Illinois, Indiana, Ohio, and Wisconsin from 1995 through 2000, six had low Sclerotinia stem rot incidence (<1%), three environments had low to moderate Sclerotinia stem rot incidence (5 to 25%), and four environments had high Sclerotinia stem rot incidence (>25%). When disease incidence was high, no consistent control of Sclerotinia stem rot was observed with benomyl or thiophanate methyl using different application systems. However, under low disease incidence, spray systems that were able to penetrate the canopy reduced the incidence of Sclerotinia stem rot an average of 50%.

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23

Pothuluri, Jairaj V., James P. Freeman, Thomas M. Heinze, Richard D. Beger, and Carl E. Cerniglia. "Biotransformation of Vinclozolin by the FungusCunninghamellaelegans." Journal of Agricultural and Food Chemistry 48, no. 12 (December 2000): 6138–48. http://dx.doi.org/10.1021/jf0008543.

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24

Yourman, L. F., S. N. Jeffers, and R. A. Dean. "Phenotype Instability in Botrytis cinerea in the Absence of Benzimidazole and Dicarboximide Fungicides." Phytopathology® 91, no. 3 (March 2001): 307–15. http://dx.doi.org/10.1094/phyto.2001.91.3.307.

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Stability of phenotypes of isolates of Botrytis cinerea that were sensitive or resistant to benzimidazole and dicarboximide fungicides was examined in the absence of fungicides in laboratory and growth room experiments. Twelve greenhouse isolates of B. cinerea were subcultured on potato dextrose agar (PDA) for 20 generations and on geranium seedlings for 15 generations. Three isolates of each of the following four phenotypes were used: sensitive to the fungicides thiophanate-methy1 (a benzimidazole) and vinclozolin (a dicarboximide) (STSV), resistant to both fungicides (RTRV), resistant to thiophanate-methy1 and sensitive to vinclozolin (RTSV), and sensitive to thiophanate-methy1 and resistant to vinclozolin (STRV). In three trials on PDA, 36 populations were subcultured; 8 populations changed phenotypes by the end of 20 generations, as determined by conidium germination on fungicide-amended medium. Five of the eight initially were STRV; the resulting phenotypes were STSV, RTSV, and RTRV. Populations from eight other isolates exhibited temporary changes in phenotype during intermediate generations on PDA but reverted to initial phenotypes by the twentieth generation; five of these populations changed to phenotype RTRV. In two geranium seedling trials, each of the 12 greenhouse isolates was inoculated onto a set of three seedlings for each generation, and diseased tissue that developed was used to initiate the next generation. Therefore, a total of 72 populations of B. cinerea were subcultured in the two trials; 5 of these populations changed phenotype at the end of 15 generations. Three of the five initially were STRV; these changed to phenotypes STSV or RTRV. In each of the two trials on geranium seedlings, a population subcultured from one STSV isolate changed phenotype one to phenotype RTRV and one to phenotype RTSV. In all trials, no population resistant to thiophanate-methy1 changed to a thiophanate-methy1-sensitive phenotype, and no population changed to phenotype STRV. Random amplified polymorphic DNA (RAPD) fingerprints were generated with the 12 initial isolates and 49 isolates subcultured on PDA or geranium seedlings. Cluster analyses of RAPD markers showed that subcultured isolates exhibiting the same phenotype clustered together and that subcultured isolates derived from a common greenhouse isolate but with different phenotypes were in different clusters. Some populations that did not change phenotype exhibited considerable differences in RAPD marker patterns. The results of this study indicate that, in the absence of fungicides, sensitive populations of B. cinerea can develop resistance to thiophanate-methy1 and vinclozolin, and this resistance can be maintained in populations through multiple generations. Populations resistant only to vinclozolin (STRV) exhibited a high frequency of phenotype change, and populations resistant to both fungicides (RTRV) were stable.

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25

James, W. H. "Is vinclozolin a reproductive hazard to men?" Occupational and Environmental Medicine 54, no. 4 (April 1, 1997): 285. http://dx.doi.org/10.1136/oem.54.4.285.

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26

Graziosi, Agnese, Giulia Sita, Camilla Corrieri, Sabrina Angelini, Roberta d’Emmanuele di Villa Bianca, Emma Mitidieri, Raffaella Sorrentino, Patrizia Hrelia, and Fabiana Morroni. "Effects of Subtoxic Concentrations of Atrazine, Cypermethrin, and Vinclozolin on microRNA-Mediated PI3K/Akt/mTOR Signaling in SH-SY5Y Cells." International Journal of Molecular Sciences 23, no. 23 (November 22, 2022): 14538. http://dx.doi.org/10.3390/ijms232314538.

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Endocrine-disrupting chemicals (EDCs) are different natural and synthetic chemicals that may interfere with several mechanisms of the endocrine system producing adverse developmental, metabolic, reproductive, and neurological effects in both human beings and wildlife. Among pesticides, numerous chemicals have been identified as EDCs. MicroRNAs (miRNAs) can regulate gene expression, making fine adjustments in mRNA abundance and regulating proteostasis. We hypothesized that exposure to low doses of atrazine, cypermethrin, and vinclozolin may lead to effects on miRNA expression in SH-SY5Y cells. In particular, the exposure of SH-SY5Y cells to subtoxic concentrations of vinclozolin is able to downregulate miR-29b-3p expression leading to the increase in the related gene expression of ADAM12 and CDK6, which may promote a pro-oncogenic response through the activation of the PI3K/Akt/mTOR pathway and counteracting p53 activity. A better understanding of the molecular mechanisms of EDCs could provide important insight into their role in human disease.

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27

Egea-González, F. J., M. L. Castro-cano, J. L. Martínez-Vidal, and M. Martínez-galera. "Analyses of Procymidone and Vinclozolin in Greenhouse Air." International Journal of Environmental Analytical Chemistry 67, no. 1-4 (June 1997): 143–55. http://dx.doi.org/10.1080/03067319708031400.

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28

Mercadier, Christine, Danielle Vega, and Jean Bastide. "Chemical and Biological Transformation of the Fungicide Vinclozolin." Journal of Agricultural and Food Chemistry 46, no. 9 (September 1998): 3817–22. http://dx.doi.org/10.1021/jf980275m.

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29

Oca, Félix Genoveva García-Montes de, Ma de Lourdes López-González, Derly Constanza Escobar-Wilches, Roberto Chavira-Ramírez, and Adolfo Sierra-Santoyo. "Vinclozolin modulates hepatic cytochrome P450 isoforms during pregnancy." Reproductive Toxicology 53 (June 2015): 119–26. http://dx.doi.org/10.1016/j.reprotox.2015.04.010.

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30

Szeto, Sunny Y., Nick E. Burlinson, James E. Rahe, and Peter C. Oloffs. "Kinetics of hydrolysis of the dicarboximide fungicide vinclozolin." Journal of Agricultural and Food Chemistry 37, no. 2 (March 1989): 523–29. http://dx.doi.org/10.1021/jf00086a055.

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31

Schwack, Wolfgang, and Beate Bourgeois. "Fungicides and photochemistry: Iprodione, procymidone, vinclozolin 1. Photodehalogenation." Zeitschrift f�r Lebensmittel-Untersuchung und -Forschung 188, no. 4 (April 1989): 346–47. http://dx.doi.org/10.1007/bf01352395.

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32

PENROSE, L. J., W. KOFFMANN, and M. R. NICHOLLS. "Field occurrence of vinclozolin resistance in Monilinia fructicola." Plant Pathology 34, no. 2 (June 1985): 228–34. http://dx.doi.org/10.1111/j.1365-3059.1985.tb01354.x.

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33

Bouchard, Dermont C. "Sorption of vinclozolin and atrazine on four geosorbents." Pesticide Science 55, no. 11 (October 15, 1999): 1095–102. http://dx.doi.org/10.1002/(sici)1096-9063(199911)55:11<1095::aid-ps61>3.0.co;2-7.

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34

Walker, Allan, Pauline A. Brown, and Andrew R. Entwistle. "Enhanced degradation of iprodione and vinclozolin in soil." Pesticide Science 17, no. 2 (April 1986): 183–93. http://dx.doi.org/10.1002/ps.2780170216.

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35

Anway, Matthew D., Charles Leathers, and Michael K. Skinner. "Endocrine Disruptor Vinclozolin Induced Epigenetic Transgenerational Adult-Onset Disease." Endocrinology 147, no. 12 (December 2006): 5515–23. http://dx.doi.org/10.1210/en.2006-0640.

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36

Schwack, Wolfgang, Frank Walker, and Beate Bourgeois. "Fungicides and photochemistry: photodegradation of the dicarboximide fungicide vinclozolin." Journal of Agricultural and Food Chemistry 43, no. 12 (December 1995): 3088–92. http://dx.doi.org/10.1021/jf00060a017.

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37

MOLINAMOLINA, J., A. HILLENWECK, I. JOUANIN, D. ZALKO, J. CRAVEDI, M. FERNANDEZ, A. PILLON, J. NICOLAS, N. OLEA, and P. BALAGUER. "Steroid receptor profiling of vinclozolin and its primary metabolites." Toxicology and Applied Pharmacology 216, no. 1 (October 1, 2006): 44–54. http://dx.doi.org/10.1016/j.taap.2006.04.005.

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38

Wu, Keyang, Yang Li, Peipei Pan, Zengqiang Li, Yige Yu, Jianjian Huang, Feifei Ma, et al. "Gestational vinclozolin exposure suppresses fetal testis development in rats." Ecotoxicology and Environmental Safety 203 (October 2020): 111053. http://dx.doi.org/10.1016/j.ecoenv.2020.111053.

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39

Vallero, Daniel A., Jerry L. Farnsworth, and J. Jeffrey Peirce. "Degradation and Migration of Vinclozolin in Sand and Soil." Journal of Environmental Engineering 127, no. 10 (October 2001): 952–57. http://dx.doi.org/10.1061/(asce)0733-9372(2001)127:10(952).

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40

Vallero, Daniel A., and J. Jeffrey Peirce. "Transformation and Transport of Vinclozolin from Soil to Air." Journal of Environmental Engineering 128, no. 3 (March 2002): 261–68. http://dx.doi.org/10.1061/(asce)0733-9372(2002)128:3(261).

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41

Schick, Bernhard, Pran N. Moza, Klaus Hustert, and Antonius Kettrup. "Photochemistry of vinclozolin in water and methanol-water solution." Pesticide Science 55, no. 11 (October 15, 1999): 1116–22. http://dx.doi.org/10.1002/(sici)1096-9063(199911)55:11<1116::aid-ps65>3.0.co;2-y.

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42

Banerjee, Anjana, Sanhita Padhi, and Tapan K. Adhya. "Persistence and biodegradation of vinclozolin in tropical rice soils." Pesticide Science 55, no. 12 (December 1999): 1177–81. http://dx.doi.org/10.1002/(sici)1096-9063(199912)55:12<1177::aid-ps70>3.0.co;2-0.

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43

Liu, Hui, Donghui Liu, Zhigang Shen, Mingjing Sun, Zhiqiang Zhou, and Peng Wang. "Chiral Separation and Enantioselective Degradation of Vinclozolin in Soils." Chirality 26, no. 3 (February 4, 2014): 155–59. http://dx.doi.org/10.1002/chir.22284.

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44

Cho, Seonghwa, Jineun Kim, Sangjin Lee, and Tae Ho Kim. "Vinclozolin: 3-(3,5-dichlorophenyl)-5-ethenyl-5-methyl-1,3-oxazolidine-2,4-dione." Acta Crystallographica Section E Structure Reports Online 70, no. 7 (June 7, 2014): o754. http://dx.doi.org/10.1107/s1600536814012781.

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In the title compound, C12H9Cl2NO3, which is the fungicide vinclozolin, the dihedral angle between the oxazolidine ring mean plane [r.m.s. deviation = 0.029 Å] and the benzene ring is 77.55 (8)°. In the crystal, molecules are linkedviaC—H...O hydrogen bonds, forming chains along [010]. The chains are linked by short Cl...Cl contacts [3.4439 (3) and 3.5798 (3) Å], resulting in a three-dimensional architecture.

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45

Hilber, Urs W., and Maja Hilber-Bodmer. "Genetic Basis and Monitoring of Resistance of Botryotinia fuckeliana to Anilinopyrimidines." Plant Disease 82, no. 5 (May 1998): 496–500. http://dx.doi.org/10.1094/pdis.1998.82.5.496.

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The anilinopyrimidines constitute a new class of mainly protective, broad-spectrum fungicides with a high activity against Botryotinia fuckeliana, the causal agent of gray mold on a wide range of host plants. The present study was initiated to investigate the genetic basis of resistance to anilinopyrimidines in B. fuckeliana and to assess the frequency of resistant isolates in vineyards in Switzerland exposed to experimental applications of anilinopyrimidines. In mating experiments, two sensitive reference isolates were crossed with three anilinopyrimidine-resistant field isolates. The analysis of 72 sexual progeny from six apothecia demonstrated that resistance to the anilinopyrimidine fungicide cyprodinil segregated in a 1:1 ratio and is therefore monogenic. The same segregation ratio was found for resistance to the dicarboximide fungicide vinclozolin. Resistance to cyprodinil segregated independently from resistance to vinclozolin. From 1993 to 1995, isolates of B. fuckeliana were collected in Switzerland from five vineyards that differed in their anilinopyrimidine spray history. Of a total of 303 isolates tested in vitro, three anilinopyrimidine-resistant isolates were detected in two vineyards where the cumulative number of treatments was between two and nine. The results of the study are discussed with respect to the implementation of an antiresistance strategy in Switzerland.

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46

Anway, M. D., M. A. Memon, M. Uzumcu, and M. K. Skinner. "Transgenerational Effect of the Endocrine Disruptor Vinclozolin on Male Spermatogenesis." Journal of Andrology 27, no. 6 (July 12, 2006): 868–79. http://dx.doi.org/10.2164/jandrol.106.000349.

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47

Mappes, D., and F. Löcher. "STRATEGIES FOR THE SAFE CONTROL OF FRUIT ROTS WITH VINCLOZOLIN." Acta Horticulturae, no. 265 (December 1989): 527–34. http://dx.doi.org/10.17660/actahortic.1989.265.78.

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48

Kodama, Shuji, Atsushi Yamamoto, Yukio Saitoh, Akinobu Matsunaga, Kazumasa Okamura, Ryoichi Kizu, and Kazuichi Hayakawa. "Enantioseparation of Vinclozolin by γ-Cyclodextrin-Modified Micellar Electrokinetic Chromatography." Journal of Agricultural and Food Chemistry 50, no. 5 (February 2002): 1312–17. http://dx.doi.org/10.1021/jf011238p.

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49

Hatzis, Alexander, and Robert Rothchild. "Binuclear NMR Shift Reagents. An Apparent Anomalous Effect with Vinclozolin." Spectroscopy Letters 19, no. 6 (July 1986): 617–26. http://dx.doi.org/10.1080/00387018608069267.

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50

Müller, R., S. Charaf, C. Scherer, A. Oppold, J. Oehlmann, and M. Wagner. "Phenotypic and epigenetic effects of vinclozolin in the gastropodPhysella acuta." Journal of Molluscan Studies 82, no. 2 (January 18, 2016): 320–27. http://dx.doi.org/10.1093/mollus/eyv069.

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