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Articles de revues sur le sujet « Testicular toxicity »

Auteur : Grafiati

Publié le 2 juin 2025

Mis à jour le 31 juillet 2025

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1

Rovira, Jordi, Fritz Diekmann, María José Ramírez-Bajo, Elisenda Bañón-Maneus, Daniel Moya-Rull, and Josep M. Campistol. "Sirolimus-Associated Testicular Toxicity." Transplantation Journal 93, no. 9 (2012): 874–79. http://dx.doi.org/10.1097/tp.0b013e31824bf1f0.

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Chatani, Fumio. "Drug-induced testicular toxicity." Folia Pharmacologica Japonica 133, no. 2 (2009): 82–86. http://dx.doi.org/10.1254/fpj.133.82.

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Mostofi, F. K. "Commentary On Testicular Toxicity." Toxicologic Pathology 25, no. 4 (1997): 418. http://dx.doi.org/10.1177/019262339702500416.

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Takahashi, Michihito, and Hajime Matsui. "Mechanisms of testicular toxicity." Journal of Toxicologic Pathology 6, no. 2 (1993): 161–74. http://dx.doi.org/10.1293/tox.6.161.

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Shigeru, Suna, and Jitsunari Fumihiko. "Effect of caffeine and ethanol intake on di (2-ethylhexyl) phthalate (DEHP)-induced testicular atrophy." World Journal of Biology Pharmacy and Health Sciences 13, no. 3 (2023): 252–61. https://doi.org/10.5281/zenodo.8036103.

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<strong>Background:</strong> Di(2-ethylhexyl) phthalate (DEHP) is the most widely used polyvinyl chloride (PVC) plasticizer. Therefore, DEHP pollution is spreading all over the world. In recent years, it has attracted attention as an endocrine disrupting chemical. In animal experiments using rodents, testicular toxicity has been confirmed by feeding diets containing DEHP. Mono(2-ethylhexyl) phthalate (MEHP), a potent oxidative stressor, is thought to be directly involved in testicular toxicity. On the other hand, caffeine and ethanol, which are hydroxyl radical scavengers, are taken in re

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Levi, Mattan, Moran Tzabari, Naphtali Savion, Salomon M. Stemmer, Ruth Shalgi, and Irit Ben-Aharon. "Dexrazoxane exacerbates doxorubicin-induced testicular toxicity." REPRODUCTION 150, no. 4 (2015): 357–66. http://dx.doi.org/10.1530/rep-15-0129.

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Infertility induced by anti-cancer treatments pose a major concern for cancer survivors. Doxorubicin (DXR) has been previously shown to exert toxic effects on the testicular germinal epithelium. Based upon the cardioprotective traits of dexrazoxane (DEX), we studied its potential effect in reducing DXR-induced testicular toxicity. Male mice were injected with 5 mg/kg DXR, 100 mg/kg DEX, combination of both or saline (control) and sacrificed either 1, 3 or 6 months later. Testes were excised and further processed. Glutathione and apoptosis assays were performed to determine oxidative stress. Im

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Gugic, Jasenka, Lorna Zadravec Zaletel, and Irena Oblak. "Treatment-related cardiovascular toxicity in long-term survivors of testicular cancer." Radiology and Oncology 51, no. 2 (2017): 221–27. http://dx.doi.org/10.1515/raon-2016-0021.

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Abstract Backgrounds Testicular cancer is the most common malignancy in young men. Considering increasing incidence, exceptionally high cure rate, as well as long life expectancy, assessment of long term toxicity in testicular cancer survivors is of great importance. In the last decades a major effort has been made in order to reduce toxicity of treatment, while maintaining its high effectiveness. Conclusions Actual knowledge on treatment toxicity is based on outdated treatment modalities. Hopefully, modern treatment modalities could reduce toxicity, but, there is no firm confirmation for that

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Aldossary, Sara Abdulraman. "Sesamol counter act toxicity of arsenic on testicular tissues." Journal of medical pharmaceutical and allied sciences 11, no. 5 (2022): 5259–63. http://dx.doi.org/10.55522/jmpas.v11i5.3794.

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The main aim of the study includes analyzing the protective effects of sesamol of testicular in arsenic-induced toxicity. Primarily there have been different treatments and sample preparation methods that includethe mixing of drugs seasonal and arsenic, as they were immersed into the aqueous solution of tween 80 and further arsenic stabilisation was done using gum of 0.2%. A total of four groups, each group having 8 rats selected. Testicular catalase is decreased in arsenic treated rats whereas testicular (Glutathione synthetase) GSH, testicular (nitric oxide) NO and testicular malondialdehyde

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Ichihara, Gaku, Nobuyuki Asaeda, Toshihiko Kumazawa, et al. "Testicular Toxicity of 2‐Bromopropane." Journal of Occupational Health 38, no. 4 (1996): 205–6. http://dx.doi.org/10.1539/joh.38.205.

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Ohara, Masao. "ULTRASTRUCTURAL STUDY OF TESTICULAR TOXICITY." Japanese Journal of Urology 79, no. 5 (1988): 788–98. http://dx.doi.org/10.5980/jpnjurol1928.79.5_788.

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AL-MOGAIREN, Sultan. "Does Abatacept Induce Testicular Toxicity?" Archives of Rheumatology 35, no. 2 (2020): 220–25. http://dx.doi.org/10.46497/archrheumatol.2020.7164.

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Frame, S. R., M. E. Hurtt, and J. W. Green. "Testicular Maturation in Prepubertal New Zealand White Rabbits." Veterinary Pathology 31, no. 5 (1994): 541–45. http://dx.doi.org/10.1177/030098589403100505.

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Testicular maturation was assessed in age-matched, sexually immature (13–17-week-old) New Zealand white rabbits using end points frequently evaluated in toxicity studies: testicular weight and testicular histology. Testicular weights and testicular maturity as assessed histologically were markedly variable in sexually immature rabbits, especially at ≥ 14 weeks of age. The large variation in testicular weights in immature rabbits requires that large changes in a treatment group relative to controls be present for statistical detection of testicular weight effects at commonly used significance l

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Shigeru Suna and Fumihiko Jitsunari. "Effect of caffeine and ethanol intake on di (2-ethylhexyl) phthalate (DEHP)-induced testicular atrophy." World Journal of Biology Pharmacy and Health Sciences 13, no. 3 (2023): 252–61. http://dx.doi.org/10.30574/wjbphs.2023.13.3.0138.

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Background: Di(2-ethylhexyl) phthalate (DEHP) is the most widely used polyvinyl chloride (PVC) plasticizer. Therefore, DEHP pollution is spreading all over the world. In recent years, it has attracted attention as an endocrine disrupting chemical. In animal experiments using rodents, testicular toxicity has been confirmed by feeding diets containing DEHP. Mono(2-ethylhexyl) phthalate (MEHP), a potent oxidative stressor, is thought to be directly involved in testicular toxicity. On the other hand, caffeine and ethanol, which are hydroxyl radical scavengers, are taken in relatively large amounts

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G.O, Adunmo, Oyewopo A.O, Akindehin O.A, et al. "Effects of phosphodiesterase 5 inhibitor (viagra) on biochemical parameters of l-name-induced testicular toxicity in adult male wistar rats." KIU Journal of Health Sciences 4, no. 1 (2024): 102–10. http://dx.doi.org/10.59568/kjhs-2024-4-1-10.

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Testicular toxicity is a growing concern in today's world, with various factors contributing to its prevalence. Nitric oxide (NO) imbalance, often induced by N (gamma)-nitro-L-arginine methyl ester (L-NAME), is a significant factor associated with testicular dysfunction. Sildenafil (Viagra), a phosphodiesterase type 5 inhibitor, has shown promise in improving testicular function by modulating NO levels. This study aimed to investigate the role of Sildenafil (Viagra) on biochemical parameters of L-NAME-induced testicular toxicity in Wistar rats. Twenty-four adult male Wistar rats were divided i

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Othman, Eman M., Heba A. Habib, Mahmoud E. Zahran, Amr Amin та Gehan H. Heeba. "Mechanistic Protective Effect of Cilostazol in Cisplatin-Induced Testicular Damage via Regulation of Oxidative Stress and TNF-α/NF-κB/Caspase-3 Pathways". International Journal of Molecular Sciences 24, № 16 (2023): 12651. http://dx.doi.org/10.3390/ijms241612651.

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Despite being a potent anticancer drug, cisplatin has limited applicability due to its adverse effects, such as testicular damage. Consequently, reducing its toxicity becomes necessary. In this study, a selective phosphodiesterase-3 inhibitor, cilostazol, which is used to treat intermittent claudication, was examined for its ability to abrogate cisplatin-induced testicular toxicity. Its ameliorative effect was compared to that of two phosphodiesterase inhibitors, tadalafil and pentoxifylline. The study also focused on the possible mechanisms involved in the proposed protective effect. Cisplati

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Kiekwe, Vershima, Gabriel Owoicho Idoko, Gabriel Godson Akunna, and Linus Chia Saalu. "Melamine and Testicular Health: Examining the Risks and Mechanisms of Toxicity." Journal of Innovations in Medical Research 3, no. 4 (2024): 13–27. https://doi.org/10.56397/jimr/2024.12.03.

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Melamine, a nitrogen-rich organic compound commonly used in industrial applications, became infamous during the 2008 Chinese milk scandal due to its association with renal damage and systemic toxicity. Its potential use as a food additive raises concerns about safety, particularly regarding reproductive health. This review examines melamine’s impact on testicular health, focusing on mechanisms of toxicity, exposure biomarkers, and public health implications. A comprehensive literature review of experimental studies, epidemiological data, and case reports was conducted to assess melamine’s effe

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Pant, Niraj, R. C. Murthy, and S. P. Srivastava. "Male reproductive toxicity of sodium arsenite in mice." Human & Experimental Toxicology 23, no. 8 (2004): 399–403. http://dx.doi.org/10.1191/0960327104ht467oa.

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The effect of chronic oral exposure to arsenic on male mouse testicular and accessory sex organ weights, sperm parameters and testicular marker enzymes was studied. In addition, the distribution of arsenic in reproductive organs was measured using atomic absorption spectrophotometry. Sodium arsenite administered to mice (Mus musculus) via drinking water at a dose of 53.39 βmol/L (4 ppm As) for 365 days caused a decrease in the absolute and relative testicular weight. However, epididymal and accessory sex organ weight was similar to control. The activities of marker testicular enzymes such as s

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Stephen, Adie Adalikwu, Uno-Ubarei Uno Ukam, Dominic Okena Ndum, Ndang Akan Anthonia, and Benjamin Ekaluo Utip. "Attenuating potential of some antioxidants: Cellgevity, max one, purslane and vitamin C on caffeine induced hormonal and testicular toxicities in male albino rats." World Journal of Advanced Research and Reviews 21, no. 1 (2024): 678–90. https://doi.org/10.5281/zenodo.13218929.

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<strong>Background</strong>: Infertility challenges in men, resulting from disturbances in hormonal balance and testicular integrity, stands as a significant health challenge associated with various factors. Consequently, diverse strategies are necessary to tackle this issue. This research explored the attenuating potentials of some antioxidants—Cellgevity (CG), Max One (MX), purslane, and vitamin C (VC)—on caffeine-induced hormonal and testicular toxicities in male albino rats. <strong>Methodology</strong>: Sixty sexually matured male albino rats were randomly divided into ten gro

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Levi, Mattan, Ruth Shalgi, and Irit Ben-Aharon. "Pretreatment with gonadotropin-releasing hormone antagonist protects against chemotherapy-induced testicular damage ‘in mice." Therapeutic Advances in Medical Oncology 14 (January 2022): 175883592211132. http://dx.doi.org/10.1177/17588359221113274.

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Background: Testicular toxicity following chemotherapy is of increasing importance with the continuous improvement of survival rates. Gonadotropin-releasing hormone (GnRH) was suggested to protect testis against such toxicity; however, its suppressive quality and mechanism of action are still unclear. We examined whether and how pretreatment with GnRH antagonist protects against the testicular damage caused by chemotherapy. Methods: Mature male mice were injected subcutaneously eight times in 2-day intervals with either saline or GnRH antagonist (Cetrotide; 1 g/mg), followed by an intraperiton

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Orisakwe, Orish Ebere, Onyenmechi Johnson Afonne, Chudi Emma Dioka, Patrick Ugochukwu Agbasi, Chukwuemeka Azikiwe, and Ejeatuluchukwu Obi. "Testicular Toxicity of Rinbacin in Rats." Biological & Pharmaceutical Bulletin 25, no. 2 (2002): 206–8. http://dx.doi.org/10.1248/bpb.25.206.

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Levi, Mattan, Aron Popovtzer, Moran Tzabari, et al. "Cetuximab intensifies cisplatin-induced testicular toxicity." Reproductive BioMedicine Online 33, no. 1 (2016): 102–10. http://dx.doi.org/10.1016/j.rbmo.2016.04.004.

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Farr, S. A., R. S. Susman, Y. C. Sunwoo, and F. E. Johnson. "Regional procarbazine delivery reduces testicular toxicity." Surgical Oncology 2, no. 6 (1993): 349–56. http://dx.doi.org/10.1016/0960-7404(93)90066-8.

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Elsharkawy, Eman E., Mahmoud Abd El-Nasser, and Heba F. Kamaly. "Silver nanoparticles testicular toxicity in rat." Environmental Toxicology and Pharmacology 70 (August 2019): 103194. http://dx.doi.org/10.1016/j.etap.2019.103194.

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Lui, Raphael C., Marie C. LaRegina, David R. Herbold, John A. Stern, and Frank E. Johnson. "Regional doxorubicin delivery reduces testicular toxicity." Journal of Surgical Research 43, no. 3 (1987): 286–95. http://dx.doi.org/10.1016/0022-4804(87)90083-7.

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John, P. J. "Nanoparticle toxicity may cause testicular dysfunction." Journal of Environmental Biology 44, no. 2 (2023): i—iii. http://dx.doi.org/10.22438/jeb/44/2/editorial.

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Nanotechnology is the science of designing, producing, and using structures and devices having one or more dimensions of about 100 millionth of a millimetre (100 nanometres) or less. It is going to be a major driving force behind the imminent technological revolution in the 21st century. Private and public sector companies are constantly in synthesizing nanomaterial based products. Nanotechnology has the potential of producing new materials and products that may revolutionize all areas of life. Meanwhile, its opponents believe that nanotechnology may cause serious health and environmental risk

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Suna, Shigeru, and Fumihiko Jitsunari. "Effects of Ethanol and Caffeine Intake on Di (2-Ethylhexyl) Phthalate (DEHP) Toxicity in Rats." Journal of Epidemiology and Public Health 3, no. 1 (2025): 01–06. https://doi.org/10.64030/3065-9078.03.01.02.

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Background: Mono(2-ethylhexyl) phthalate (MEHP), a metabolite of di(2-ethylhexyl) phthalate (DEHP), stimulates peroxisome proliferator-activated receptors and disrupts carbohydrate and lipid metabolism. The oxidative stress generated may be closely related to the toxicity of DEHP. The authors report on the effects of simultaneous consumption of drinking water containing the hydroxyl radical scavengers’ ethanol or caffeine on diet-mediated DEHP toxicity. Method: Four-week-old male SD rats were divided into control, DEHP, DEHP+ethanol and DEHP+caffeine groups (6 rats per group). The treatment gr

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Fouad, Amr A., Waleed H. Albuali, Abdulruhman S. Al-Mulhim, and Iyad Jresat. "Protective effect of telmisartan treatment against arsenic-induced testicular toxicity in rats." Zeitschrift für Naturforschung C 70, no. 7-8 (2015): 175–81. http://dx.doi.org/10.1515/znc-2015-5031.

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Abstract Oxidative/nitrosative stress, inflammation, and apoptosis play a crucial role in the pathogenesis of arsenic-induced testicular injury. Telmisartan, the angiotensin II-receptor antagonist, possesses antioxidant and anti-inflammatory activities. The protective effect of telmisartan against arsenic-induced testicular damage was investigated in rats. Testicular damage was induced by sodium arsenite (10 mg kg–1/day, p.o., for 2 consecutive days). Telmisartan (10 mg kg–1/day, i.p.) was given for 3 consecutive days, starting 1 day before sodium arsenite administration. Telmisartan significa

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Kumar, P., A. K. Prasad, U. Mani, B. K. Maji, and K. K. Dutta. "Trichloroethylene induced testicular toxicity in rats exposed by inhalation." Human & Experimental Toxicology 20, no. 11 (2001): 585–89. http://dx.doi.org/10.1191/096032701718620882.

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Trichloroethylene (TCE) is an organic solvent used in dry cleaning, metal degreasing, thinner for paints and varnishes, anesthetic agent, and so forth. Human beings are appreciably exposed to TCE vapours by inhalation route. The present study has been undertaken to investigate whether TCE inhalation may also bring about testicular toxic effects. Our results indicate that inhalation of TCE by male rats for 12 and 24 weeks brings about significant reduction in absolute testicular weight, and alters marker testicular enzymes activity associated with spermatogenesis and germ cell maturation, along

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Creasy, D. M., and R. E. Chapin. "Testicular and epididymal toxicity: Pathogenesis and potential mechanisms of toxicity." Spermatogenesis 4, no. 2 (2014): e1005511. http://dx.doi.org/10.1080/21565562.2014.1005511.

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Wahba, Zakaria Z., Mark Steven Miller, and Michael P. Waalkes. "Absence of Changes in Metallothionein RNA in the Rat Testes Made Refractory to Cadmium Toxicity by Zinc Pretreatment." Human & Experimental Toxicology 13, no. 1 (1994): 65–67. http://dx.doi.org/10.1177/096032719401300110.

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Testicular toxicity and interstitial cell tumours induced by cadmium are prevented by zinc or by low dose cadmium pretreatments. The mechanism of this tolerance is unknown, though metallothionein (MT) is thought to play a role in tissue resistance to cadmium toxicity. Thus, the possible involvement of the testicular MT gene in metal-induced tolerance to cadmium toxicity was studied. Rats were pretreated with zinc (1.0 mmol kg-1, s.c.). Histological examination of the testes indicated such pretreatments prevented the necrotizing effects of subsequent doses of cadmium (20 ?mol kg-1, s.c.) admini

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Lent, Emily May, Lee C. B. Crouse, and Shannon M. Wallace. "Oral Toxicity of 2,4-Dinitroanisole in Rats." International Journal of Toxicology 35, no. 6 (2016): 692–711. http://dx.doi.org/10.1177/1091581816670321.

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Subacute and subchronic studies were conducted to assess the toxicity of 2,4-dinitroanisole (DNAN) and to provide information important for protecting the health of military and civilian personnel. In the subchronic study, male and female Sprague-Dawley rats were dosed with DNAN via oral gavage at 0, 1.25, 5, 20, and 80 mg/kg/d. Likely owing to its conversion to 2,4-dinitrophenol, an inhibitor of energy homeostasis, DNAN caused an apparent increase in metabolism, leading to reduced feed efficiency ratios and body mass gains in males. Anemia, splenic enlargement, hemosiderosis, and extramedulla

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Akinjo, Oluwajoba O., Timothy W. Gant, and Emma L. Marczylo. "Perturbation of microRNA signalling by doxorubicin in spermatogonial, Leydig and Sertoli cell lines in vitro." Toxicology Research 7, no. 5 (2018): 760–70. http://dx.doi.org/10.1039/c7tx00314e.

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Doxorubicin-induced testicular toxicity involves perturbation of microRNAs within all three of the main testicular cell types, particularly those involved in germ–Sertoli and Sertoli–Sertoli cell junctions.

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Alshehri, Fahad S. "Resveratrol Ameliorates Vancomycin-Induced Testicular Dysfunction in Male Rats." Medicina 59, no. 3 (2023): 486. http://dx.doi.org/10.3390/medicina59030486.

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Background and Objectives: Numerous studies have indicated that antibiotics may adversely affect testicular and sperm function. As an alternative to penicillin, vancomycin is a glycopeptide antibiotic developed to treat resistant strains of Staphylococcus aureus. A few studies have suggested that vancomycin could cause testicular toxicity and apoptosis. Vancomycin, however, has not been investigated in terms of its mechanism of causing testicular toxicity. Materials and Methods: An experiment was conducted to investigate the effects of resveratrol (20 mg/kg, oral gavage) against vancomycin (20

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Shigeru, Suna* and Masaaki Tokuda. "Effect of D-allulose on di-n-butyl phthalate (DBP) toxicity in rats." International Journal of Pharmaceutical Science and Health Care 15, no. 3 (2025): 10–18. https://doi.org/10.5281/zenodo.15535292.

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<strong>Abstract</strong> <strong>Background</strong>: Oral exposure to high concentrations of di-n-butyl phthalate (DBP) causes testicular and hepatotoxicity in rodents. DBP-metabolite, mono-n-butyl phthalate (MBP) stimulates peroxisome proliferator-activated receptors and disrupts carbohydrate and lipid metabolism. The oxidative stress generated may be closely related to these toxicities. <strong>Method</strong>: To determine the effect of D-allulose on DBP-induced testicular and hepatotoxicity, rats were fed a DBP (1% or 2%) diet and D-allulose (2%) in the drinking water. <strong>Result</st

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Briseño-Bugarín, Jorge, Isabel Hernández-Ochoa, Xelha Araujo-Padilla, et al. "Phycobiliproteins Ameliorate Gonadal Toxicity in Male Mice Treated with Cyclophosphamide." Nutrients 13, no. 8 (2021): 2616. http://dx.doi.org/10.3390/nu13082616.

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Cyclophosphamide (CP)—which is used to treat autoimmune diseases and cancer—is related to gonadotoxicity attributed to oxidative stress. As phycobiliproteins (PBPs) are strong antioxidants that are unexplored as protective agents against male gonadotoxicity, our work aimed to investigate the effects of PBP crude extract on testicular damage and sperm parameter alterations caused by CP in mice. Three doses of PBP (50, 100, and 200 mg/kg) were tested in the experimental groups (n = 8 per group), administered concomitantly with 100 mg/kg CP. After 42 days receiving PBP daily and CP weekly, body a

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Melebary, Sahar J. "The Possible Protective Effect of Luteolin in a Thioacetamide Rat Model of Testicular Toxicity." International Journal of Agriculture and Biology 28, no. 06 (2022): 391–404. http://dx.doi.org/10.17957/ijab/15.1993.

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Luteolin is a flavone that serves as a natural antioxidant. The therapeutic impacts of luteolin is influenced by its antioxidant, anti-inflammatory, anticancer, neuroprotective and antineoplastic properties. This study aimed to establish an animal model of testicular toxicity caused by Thioacetamide (TAA). In addition, high doses of Luteolin (LUT) were supplemented to observe the role of LUT in attenuating spermato-toxicity, the hazard of oxidative stress, and testicular histopathological alterations induced by TAA. Thirty adult rats were equally divided into three groups as follow; G1: negati

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Sherif, Iman O., and Osama M. Sarhan. "Candesartan in a rat model of testicular toxicity: New insight on its protective mechanism." Experimental Biology and Medicine 244, no. 7 (2019): 593–601. http://dx.doi.org/10.1177/1535370219842149.

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Cisplatin (CDDP) is widely used as an effective chemotherapy; nevertheless, its use is associated with male reproductive system damage. Candesartan (Cand) is an angiotensin II receptor blocker which showed a protective effect against CDDP-induced testicular toxicity. This study was implemented to investigate further novel molecular protective effect of Cand. Animals were divided into four groups and treated for 10 days as: Group I (Normal control): received saline, Group II (Cand control): treated with Cand (10 mg/kg/day) orally, Group III (CDDP): injected with a single dose of 10 mg/kg CDDP i

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Mouro, Viviane G. S., Ana L. P. Martins, Janaina Silva, et al. "Subacute Testicular Toxicity to Cadmium Exposure Intraperitoneally and Orally." Oxidative Medicine and Cellular Longevity 2019 (November 25, 2019): 1–14. http://dx.doi.org/10.1155/2019/3429635.

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The toxic effects of cadmium (Cd) on reproductive parameters are widely described in the literature. Experimental models often make use of the intraperitoneal route (i.p.), although human intoxication occurs preferentially by the oral route and can be continuous. However, little is known about the effect of Cd administration routes on the testicular structure. Thus, this study investigated the testicular impact of Cd exposure comparing both i.p. and oral routes, both single dose (SD), in addition to the oral route in fractional doses (FD). Swiss adult male mice received CdCl2 1.5 mg/kg i.p., 3

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Amin, Amr, Christeena Abraham, Alaaeldin A. Hamza, et al. "A Standardized Extract ofGinkgo bilobaNeutralizes Cisplatin-Mediated Reproductive Toxicity in Rats." Journal of Biomedicine and Biotechnology 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/362049.

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The aim of this study was to evaluate the protective effects ofGinkgo biloba(GB) against testicular damage and oxidative stress as well as caudal sperm indices in a cisplatin- (CIS-) induced rodent model. Adult male Wistar rats were given vehicle, single i.p. dose of CIS alone (10 mg/kg), GB alone (200 mg g/kg every day for five days), or single dose of CIS followed by GB (50, 100, or 200 mg/kg every day for five days). On day 6, after the first drug treatment oxidative and apoptotic testicular toxicity was evaluated. CIS-treated rats displayed decreased weights of testes and epididymis as wel

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Vasistha, Aman, Rishi Kothari, Adarsh Mishra, Fernando De Andrés, Adrián LLerena, and Sujit Nair. "Current Insights into Interethnic Variability in Testicular Cancers: Population Pharmacogenetics, Clinical Trials, Genetic Basis of Chemotherapy- Induced Toxicities and Molecular Signal Transduction." Current Topics in Medicinal Chemistry 20, no. 20 (2020): 1824–38. http://dx.doi.org/10.2174/1568026620666200618112205.

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Testicular cancer is an aggressive malignancy with a rising incidence rate across the globe. Testicular germ cell tumors are the most commonly diagnosed cancers, and surgical removal of the testes is often a radical necessity along with chemotherapy and radiotherapy. While seminomas are receptive to radiotherapy as well as chemotherapy, non-seminomatous germ cell tumors respond to chemotherapy only. Due to the singular nature of testicular cancers with associated orchiectomy and mortality, it is important to study the molecular basis and genetic underpinnings of this group of cancers across ma

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Negm, Walaa, Aya H. El-Kadem, Ismail A. Hussein, and Moneerah J. Alqahtani. "The Mechanistic Perspective of Bilobetin Protective Effects against Cisplatin-Induced Testicular Toxicity: Role of Nrf-2/Keap-1 Signaling, Inflammation and Apoptosis." Biomedicines 10, no. 5 (2022): 1134. http://dx.doi.org/10.3390/biomedicines10051134.

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Cisplatin (CP) is a productive anti-tumor used to treat numerous tumors. However, multiple toxicities discourage prolonged use, especially toxicity on the reproductive system. This experiment was mapped out to determine the potential therapeutic impact of Bilobetin on CP-induced testicular damage. Herein, Bilobetin was isolated from Cycas thouarsii leaves R. Br ethyl acetate fractions for the first time. A single dose of CP (7 mg/kg, IP) was used to evoke testicular toxicity on the third day. Rats were classified into five groups; Normal control, Bilobetin 12 mg/kg, Untreated CP, and CP treate

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Ben-Aharon, Irit, Moran Tzabari, Naftaly Savion, Ruth Shalgi, and Salomon M. Stemmer. "Effect of dexrazoxane on doxorubicin-induced testicular toxicity." Journal of Clinical Oncology 30, no. 15_suppl (2012): 2556. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.2556.

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2556 Background: Seminal advances in anti-cancer therapy result in growing numbers of young male cancer survivors for whom treatment-induced infertility represents a major late-term concern. Doxorubicin (DXR) has been previously shown to exert toxic effect on the testicular germinal epithelium. Based upon the cardioprotective traits of dexrazoxane (DEX), we aimed to study its potential effect to reduce DXR-induced testicular toxicity. Methods: Male mice were injected intraperitoneally with 5mg/kg DXR or 100mg/kg DEX or the combination of both and scarified at one month post treatment. Saline-i

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Vidal, Justin D., and Katharine M. Whitney. "Morphologic manifestations of testicular and epididymal toxicity." Spermatogenesis 4, no. 2 (2014): e979099. http://dx.doi.org/10.4161/21565562.2014.979099.

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Stoll, R. E. "Symposium on Testicular Toxicity and Neoplasia: Introduction." Journal of the American College of Toxicology 8, no. 3 (1989): 455. http://dx.doi.org/10.3109/10915818909014531.

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Omura, Minoru, Akiyo Tanaka, Miyuki Hirata, et al. "Testicular Toxicity Evaluation of Indium‐Tin Oxide." Journal of Occupational Health 44, no. 2 (2002): 105–7. http://dx.doi.org/10.1539/joh.44.105.

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OMURA, Minoru, Akiyo TANAKA, Miyuki HIRATA, et al. "Testicular Toxicity Evaluation of Indium-Tin Oxide." SANGYO EISEIGAKU ZASSHI 44, no. 2 (2002): A23. http://dx.doi.org/10.1539/sangyoeisei.kj00002552773.

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Prahalathan, Chidambaram, Elangovan Selvakumar, and Palaninathan Varalakshmi. "Lipoic acid modulates adriamycin-induced testicular toxicity." Reproductive Toxicology 21, no. 1 (2006): 54–59. http://dx.doi.org/10.1016/j.reprotox.2005.07.002.

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Formigli, L., R. Scelsi, P. Poggi, et al. "Thallium-induced testicular toxicity in the rat." Environmental Research 40, no. 2 (1986): 531–39. http://dx.doi.org/10.1016/s0013-9351(86)80128-1.

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Whitney, Katharine M. "Testicular histopathology in juvenile rat toxicity studies." Systems Biology in Reproductive Medicine 58, no. 1 (2012): 51–56. http://dx.doi.org/10.3109/19396368.2011.647380.

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Ward, Jerry Ann, Janet Robinson, and Ian D. Morris. "Strain-dependency of procarbazine-induced testicular toxicity." Reproductive Toxicology 3, no. 1 (1989): 43–50. http://dx.doi.org/10.1016/0890-6238(89)90037-3.

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