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Journal articles on the topic 'Methylclofenapate'

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Published: 4 June 2021

Last updated: 11 February 2022

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1

Bell, D. R., N. J. Plant, C. G. Rider, L. Na, S. Brown, I. Ateitalla, S. K. Acharya, et al. "Species-specific induction of cytochrome P-450 4A RNAs: PCR cloning of partial guinea-pig, human and mouse CYP4A cDNAs." Biochemical Journal 294, no. 1 (August 15, 1993): 173–80. http://dx.doi.org/10.1042/bj2940173.

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PCR was used to demonstrate the presence of a conserved region and to clone novel members of the cytochrome P-450 4A gene family from guinea pig, human and mouse cDNAs. This strategy is based on the sequences at nucleotides 925-959 and at the haem binding domain (nucleotides 1381-1410) of the rat CYP4A1 gene. Murine Cyp4a clones showed high sequence identity with members of the rat gene family, but CYP4A clones from human and guinea pig were equally similar to the rat/mouse genes, suggesting that the rat/mouse line had undergone gene duplication events after divergence from human and guinea-pig lines. The mouse Cyp4a-12 clone was localized to chromosome 4 using interspecific backcross mapping, in a region of synteny with human chromosome 1. The assignment of the human CYP4A11 gene to chromosome 1 was confirmed by somatic cell hybridization. An RNAase protection assay was shown to discriminate between the murine Cyp4a-10 and Cyp4a-12 cDNAs. Treatment of mice with the potent peroxisome proliferator methylclofenapate (25 mg/kg) induced Cyp4a-10 RNA in liver, and to a lesser extent in kidney; there was no sex difference in this response. Cyp4a-12 RNA was present at high levels in male control liver and kidney samples, and was not induced by treatment with methylclofenapate. However, Cyp4a-12 RNA was present at low levels in control female liver and kidney RNA, and was greatly induced in both organs by methylclofenapate. Guinea pigs were exposed to methylclofenapate (50 mg/kg), but there was no significant induction of the guinea-pig CYP4A13 RNA. These findings are consistent with a species difference in response to peroxisome proliferators between the rat/mouse and the guinea pig.

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2

Bell, D. R., R. G. Bars, G. G. Gibson, and C. R. Elcombe. "Localization and differential induction of cytochrome P450IVA and acyl-CoA oxidase in rat liver." Biochemical Journal 275, no. 1 (April 1, 1991): 247–52. http://dx.doi.org/10.1042/bj2750247.

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The peroxisome proliferators are structurally diverse chemicals which induce hyperplasia, hypertrophy and the proliferation of peroxisomes in the rodent liver. Cytochrome P450IVA1 and peroxisomal enzymes, such as acyl-CoA oxidase, are induced and are early markers of treatment with peroxisome proliferators. In this study, rats were dosed intraperitoneally with the potent peroxisome proliferator methylclofenapate and the hepatic induction response was studied. There was no significant change in the enzyme activities of laurate hydroxylase (cytochrome P450IVA1) or acyl-CoA oxidase in the first 8 h after treatment, but the activities had doubled at 24 h, suggesting that these enzymes are not involved in the mediation of early events in peroxisome proliferation. Hepatic cytochrome P450IVA1 mRNA was significantly increased at 6 and 8 h after treatment, rising to 15-fold above control values at 30 h. In contrast, acyl-CoA oxidase mRNA showed no significant change in the first 8 h, but increased to 13-fold above control values at 24 and 30 h, thereby demonstrating different kinetics of induction of the two mRNAs. In order to determine whether cytochrome P450IVA1 and peroxisomal enzymes were included in the same cells, rats were treated daily with sub-maximal (2 or 5 mg/kg) and maximal (25 mg/kg) inducing doses of methylclofenapate for 4 days. The lobular distribution of induced proteins was determined immunocytochemically with antibodies raised against P450IVA1 and acyl-CoA oxidase. Livers from control animals showed minimal staining for both proteins. However, in the livers of animals treated with 2 or 5 mg of methylclofenapate/kg, both acyl-CoA and P450IVA immunostaining was increased, mainly in the centrilobular area. Immunostaining of serial sections revealed that these proteins were induced in the same region of the lobule. A maximal inducing dose of methylclofenapate (25 mg/kg) caused panlobular induction of both proteins. The results demonstrate that these proteins are induced in a dose-dependent manner in the same, spatially distinct, sensitive region of the liver lobule.

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3

Bell, D. R., and C. R. Elcombe. "Induction of acyl-CoA oxidase and cytochrome P450IVA1 RNA in rat primary hepatocyte culture by peroxisome proliferators." Biochemical Journal 280, no. 1 (November 15, 1991): 249–53. http://dx.doi.org/10.1042/bj2800249.

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We have characterized the induction of acyl-CoA oxidase and cytochrome P450IVA1 RNAs in a primary hepatocyte culture system in vitro, using a sensitive and specific RNAse protection assay. Hepatocytes were cultured with a maximal inducing dose of the peroxisome proliferator clofibric acid (1 mM), or vehicle control, for 4 days, and the level of RNAs compared with the level in rats which had been treated with corn oil or clofibric acid (300 mg/kg) for 4 days. The level of acyl-CoA oxidase and P450IVA1 RNAs in 4-day-old control hepatocytes was less than 2% of that in control liver. However, the level of these RNAs in RNA from treated hepatocytes was 61% of that in liver RNA from treated rats. Hepatocytes were treated with the potent peroxisome proliferator methylclofenapate (100 microM), and the induction of RNAs determined at various times after exposure. P450IVA1 RNA was significantly induced 1 h after dosing, rising to 34-fold above control after 8 h, whereas acyl-CoA oxidase RNA was not significantly induced until 4 h, increasing to 5.2-fold above control after 8 h. A similar time course of induction was seen after treatment of hepatocytes with 100 microM-nafenopin, 100 microM-methylclofenapate, 1 mM-clofibric acid or 1 mM-mono(ethylhexyl) phthalate, suggesting that the differential time course of induction of P450IVA1 and acyl-CoA oxidase RNAs is not related to the esterification, structure or potency of the peroxisome proliferator, but is intrinsic to the process of peroxisome proliferation. Hepatocytes were treated with methylclofenapate in the presence and absence of cycloheximide. P450IVA1 RNA was significantly induced by methylclofenapate in the presence of cycloheximide, rising to 17-fold above control after 8 h. However, no induction of acyl-CoA oxidase RNA was detected in the presence of cycloheximide. Therefore we characterize the induction of acyl-CoA oxidase and P450IVA1 RNAs in primary hepatocyte culture in vitro as a faithful model of the induction response in rat liver, and suggest that induction of P450IVA1 RNA is a primary event in the process of peroxisome proliferation.

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4

Bybee, A., J. A. Styles, S. L. Beck, and D. Blackburn. "Mitosis and histopathology in rat liver during methylclofenapate-induced hyperplasia." Cancer Letters 52, no. 2 (July 1990): 95–100. http://dx.doi.org/10.1016/0304-3835(90)90250-2.

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5

Lake, Brian G., Paul C. Rumsby, Morag E. Cunninghame, and Roger J. Price. "Dose-related effects of the peroxisome proliferator methylclofenapate in rat liver." Environmental Toxicology and Pharmacology 11, no. 3-4 (July 2002): 233–42. http://dx.doi.org/10.1016/s1382-6689(01)00116-8.

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6

Styles, J. A., M. D. Kelly, N. R. Pritchard, and C. R. Elcombe. "A Species Comparison of Acute Liver Hyperplasia Induced by the Peroxisome Proliferator Methylclofenapate." Human Toxicology 7, no. 4 (July 1988): 372. http://dx.doi.org/10.1177/096032718800700415.

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7

Styles, J. A., M. D. Kelly, C. R. Elcombe, A. Bybee, and N. R. Pritchard. "Recovery of hyperplastic responsiveness in rat liver after dosing with the peroxisome proliferator methylclofenapate." Carcinogenesis 12, no. 11 (1991): 2127–33. http://dx.doi.org/10.1093/carcin/12.11.2127.

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8

Hasmall, Susan C., and Ruth A. Roberts. "The Nongenotoxic Hepatocarcinogens Diethylhexylphthalate and Methylclofenapate Induce DNA Synthesis Preferentially in Octoploid Rat Hepatocytes." Toxicologic Pathology 28, no. 4 (July 2000): 503–9. http://dx.doi.org/10.1177/019262330002800401.

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9

Styles, J. A., M. Kelly, N. R. Pritchard, and C. R. Ekcombe. "A species comparison of acute hyperplasia induced by the peroxisome proliferator methylclofenapate: involvement of the binucleated hepatocyte." Carcinogenesis 9, no. 9 (1988): 1647–55. http://dx.doi.org/10.1093/carcin/9.9.1647.

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10

BELL, Alex R., Richard SAVORY, Neill J. HORLEY, Agharul I. CHOUDHURY, Maurice DICKINS, Tim J. B. GRAY, Andrew M. SALTER, and David R. BELL. "Molecular basis of non-responsiveness to peroxisome proliferators: the guinea-pig PPARα is functional and mediates peroxisome proliferator-induced hypolipidaemia." Biochemical Journal 332, no. 3 (June 15, 1998): 689–93. http://dx.doi.org/10.1042/bj3320689.

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The guinea pig does not undergo peroxisome proliferation in response to peroxisome proliferators, in contrast with other rodents. To understand the molecular basis of this phenotype, the peroxisome proliferator activated receptor α (PPARα) from guinea-pig liver was cloned; it encodes a protein of 467 amino acid residues that is similar to rodent and human PPARα. The guinea-pig PPARα showed a high substitution rate: maximum likelihood analysis was consistent with rodent monophyly, but could not exclude rodent polyphyly (P≈ 0.06). The guinea-pig PPARα cDNA was expressed in 293 cells and mediated the induction of the luciferase reporter gene by the peroxisome proliferator, Wy-14,643, dependent on the presence of a peroxisome proliferator response element. Moreover the PPARα RNA and protein were expressed in guinea-pig liver, although at lower levels than in a species which is responsive to peroxisome proliferators, the mouse. To determine whether the guinea-pig PPARα mediated any physiological effects, guinea pigs were exposed to two selective PPARα agonists, Wy-14,643 and methylclofenapate; both compounds induced hypolipidaemia. Thus the guinea pig is a useful model for human responses to peroxisome proliferators.

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11

Barrass, N. C., R. J. Price, B. G. Lake, and T. C. Orton. "Comparison of the acute and chronic mitogenic effects of the peroxisome proliferators methylclofenapate and clofibric acid in rat liver." Carcinogenesis 14, no. 7 (1993): 1451–56. http://dx.doi.org/10.1093/carcin/14.7.1451.

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12

Miller, Richard T., Rekha S. Shah, Russell C. Cattley, and James A. Popp. "The Peroxisome Proliferators WY-14,643 and Methylclofenapate Induce Hepatocyte Ploidy Alterations and Ploidy-Specific DNA Synthesis in F344 Rats." Toxicology and Applied Pharmacology 138, no. 2 (June 1996): 317–23. http://dx.doi.org/10.1006/taap.1996.0130.

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13

Styles, J. A., M. D. Kelly, N. R. Pritchard, and J. R. Foster. "Effects produced by the non-genotoxic hepatocarcinogen methylclofenapate in dwarf mice: peroxisome induction uncoupled from DNA synthesis and nuclearity changes." Carcinogenesis 11, no. 3 (1990): 387–91. http://dx.doi.org/10.1093/carcin/11.3.387.

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14

Plant, N. "The coordinate regulation of DNA synthesis and suppression of apoptosis is differentially regulated by the liver growth agents, phenobarbital and methylclofenapate." Carcinogenesis 19, no. 9 (September 1, 1998): 1521–27. http://dx.doi.org/10.1093/carcin/19.9.1521.

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15

Garcia-Allan, C., J. Loughlin, T. Orton, and P. Lord. "Changes in protein and mRNA levels of growth factor/growth factor receptors in rat livers after administration of phenobarbitone or methylclofenapate." Archives of Toxicology 71, no. 7 (May 30, 1997): 409–15. http://dx.doi.org/10.1007/s002040050404.

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16

McQuaid, S., S. E. H. Russell, S. A. Withe, C. M. Fearson, C. R. Elcombe, and P. Humphries. "Analysis of transcripts homologous to acyl-CoA oxidase and enoyl-CoA hydratase 3-hydroxyacyl-CoA dehydrogenase induced in rat liver by methylclofenapate." Cancer Letters 37, no. 1 (October 1987): 115–21. http://dx.doi.org/10.1016/0304-3835(87)90152-2.

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17

Auton, T. R., M. A. Kelly, and J. A. Styles. "A mathematical model for the cellular dynamics and labelling kinetics governing the response of rat, mouse, hamster and guinea pig hepatocytes to methylclofenapate." Mathematical and Computer Modelling 14 (1990): 604–9. http://dx.doi.org/10.1016/0895-7177(90)90253-j.

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18

HENG, Yee M., C. W. Sharon KUO, Paul S. JONES, Richard SAVORY, Ruth M. SCHULZ, Simon R. TOMLINSON, Tim J. B. GRAY, and David R. BELL. "A novel murine P-450 gene, Cyp4a14, is part of a cluster of Cyp4a and Cyp4b, but not of CYP4F, genes in mouse and humans." Biochemical Journal 325, no. 3 (August 1, 1997): 741–49. http://dx.doi.org/10.1042/bj3250741.

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Genomic clones for Cyp4a12 and a novel member of the murine Cyp4a gene family were isolated. The novel gene, designated Cyp4a14, has a GC rich sequence immediately 5′ of the transcription start site, and is similar to the rat CYP4A2 and CYP4A3 genes. The Cyp4a14 gene spans approximately 13 kb, and contains 12 exons; sequence similarity to the rat CYP4A2 gene sequence falls off 300 bp upstream from the start site. In view of the known sex-specific expression of the rat CYP4A2 gene, the expression and inducibility of Cyp4a14 was examined. The gene was highly inducible in the liver when mice were treated with the peroxisome proliferator, methylclofenapate; induction levels were low in control animals and no sex differences in expression were observed. By contrast, the Cyp4a12 RNA was highly expressed in liver and kidney of control male mice but was expressed at very low levels in liver and kidney of female mice. Testosterone treatment increased the level of this RNA in female liver slightly, and to a greater extent in the kidney of female mice. In agreement with studies on the cognate RNA, expression of Cyp4a12 protein was male-specific in the liver of control mice and extremely high inducibility of Cyp4a10 protein, with no sex differences, was also demonstrated. In view of the overlapping patterns of inducibility of the three Cyp4a genes, we investigated whether the three genes were co-localized in the genome. Two overlapping yeast artificial chromosome (YAC) clones were isolated, and the three Cyp4a genes were shown to be present on a single YAC of 220 kb. The Cyp4a genes are adjacent to the Cyp4b1 gene, with Cyp4a12 most distant from Cyp4b1. The clustering of these two gene subfamilies in the mouse was replicated in the human, where the CYPA411 and CYP4B1 genes were present in a single YAC clone of 440 kb. However, the human CYP4F2 gene was mapped to chromosome 19. Phylogenetic analysis of the CYP4 gene families demonstrated that CYP4A and CYP4B are more closely related than CYP4F.

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19

Lefevre, P. A., H. Tinwell, S. M. Galloway, R. Hill, J. M. Mackay, C. R. Elcombe, J. Foster, V. Randall, R. D. Callander, and J. Ashby. "Evaluation of the Genetic Toxicity of the Peroxisome Proliferator and Carcinogen Methyl Clofenapate, Including Assays Usin Muta TM Mouse and Big Blue™ Transgenic Mice." Human & Experimental Toxicology 13, no. 11 (November 1994): 764–75. http://dx.doi.org/10.1177/096032719401301105.

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The rodent liver carcinogen and hepatic peroxisome proliferator methylclofenapate (MCP) has been evaluated for genetic toxicity in a range of in vitro and rodent genotoxicity assays. It gave a negative response in each of the following assays: mutagenicity to S.typhimurium and E.coli (± S9 mix, plate and pre-incubation assays), clastogenicity to cultured human lymphocytes and CHO cells (± S9 mix), a mouse bone marrow micronucleus assay (24h and 48h sampling), a rat liver assay for UDS in vivo (12h sampling), assays for lac I (Big Blue™) and lac Z (Muta™ Mouse) mutations in the liver of transgenic mice, and an assay of the ability of MCP to modify the mutagenicity to the liver of dimethylnitrosamine in both transgenic mutation assays. The micronucleus and UDS assays were conducted using a single administration of MCP at its maximum tolerated dose, while the transgenic assays were conducted using nine daily administrations of MCP at its cancer bioassay dose level. These nine daily administrations were shown to double the weight of the liver of non-transgenic, Big Blue™ and Muta™ Mice, as well as leading to a dramatic proliferation of peroxisomes (electron microscopy) in the livers of each strain. These changed parameters had returned to control levels when the mutation analyses were conducted (10 days after the final dose of MCP). Despite the liver enlargement observed following MCP administration, no evidence of mitotic activity was observed in treated livers, although an increased number of cells were undergoing replicative DNA synthesis during the final 3 days of the 9 days of administration (BUdR assessment of S-phase). Liver biochemistry parameters (ALT, AST, AP, CK, GGT and albumin) were unaffected by the chronic (9 day) administration of MCP indicating an absence of hepatic toxicity, These combined observations favour a non-genotoxic mechanism of action for the hepatic carcinogenicity of MCP. The clastogenicity in vitro of the peroxisome proliferator Wyeth 14,643 has been confirmed in CHO cells, but it is noted that this chemical is more soluble than is MCP. In particular, at the highest dose level at which MCP could be tested, Wy 14,643 was also nonclastogenic.

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