Aktivierung von Mikrosomenenzymen durch Hexachlorcyclohexan-Isomere. Ihr Einflu� auf die Scillirosidvergiftung der Ratte

Koransky, W.; Portig, J.; Vohland, H. W.; Klempau, I.

doi:10.1007/bf00246342

Cited by 32 publications

(4 citation statements)

References 11 publications

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“…Hyperplastic nodules and carcinomas in the livers of rats and mice were found induced by the longterm administration of high doses of α-BHC (such as 500 or 1000 ppm), but not β-and γ-BHC 50,51 . Furthermore, early toxicological studies revealed that α-, β-, and γ-BHC are potent inducers of hepatic monooxygenases in rats 52 , in addition to causing liver enlargement 53,54 . Since induction of the monooxygenase system is assumed to influence the p r o m o t i o n s t a g e 5 5 , 5 6 , t h e m e c h a n i s m o f α -B H C carcinogenicity is likely to be due to its influence on spontaneously initiated hepatocytes 50,51 .…”

Section: Threshold In Phenobarbital Hepatocarcinogenicitymentioning

confidence: 99%

Hormesis in Carcinogenicity of Non-genotoxic Carcinogens

et al. 2006

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Abstract:Recently the idea of hormesis, a biphasic dose-response relationship in which a chemical exerts opposite effects dependent on the dose, has attracted interest in the field of carcinogenesis. With non-genotoxic agents there is considerable experimental evidence in support of hormesis and the present review highlights current knowledge of doseresponse effects. In particular, several in vivo studies have provided support for the idea that non-genotoxic carcinogens may inhibit hepatocarcinogenesis at low doses. Here, we survey the examples and discuss possible mechanisms of hormesis with cytochrome P450 inducers, such as phenobarbital, 1,1-bis(p-chlorophenyl)-2,2,2-trichloroethane (DDT), α-benzene hexachloride (α-BHC), and other non-genotoxins. Epigenetic processes differentially can be affected by agents that impinge on oxidative stress, DNA repair, cell proliferation, apoptosis, intracellular communication and cell signaling. Non-genotoxic carcinogens may target nuclear receptors, cause aberrant DNA methylation at the genomic level and induce post-translational modifications at the protein level, thereby impacting on the stability or activity of key regulatory proteins, including oncoproteins and tumor suppressor proteins. Via multiple epigenetic lesions, nongenotoxic carcinogens can elicit a variety of changes contributing to cellular carcinogenesis. (J Toxicol Pathol 2006; 19: 111-122)

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Section: Threshold In Phenobarbital Hepatocarcinogenicitymentioning

confidence: 99%

Hormesis in Carcinogenicity of Non-genotoxic Carcinogens

et al. 2006

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“…These durations do not correlate with the relative storage levels of the isomers of BHC in rat fat as reported by DAVIDOW and FRAWLEY (1951). KORANSKY et al (1964) also showed that this BHC-induced enzyme stimulation made rats more refractory to poisoning by scillicoside, the active principle of the rodenticide red squill. The BHC-induced tolerance to scillicoside could be abolished by CFT 1201 or ethionine.…”

Section: B) Organochlorine Compoundsmentioning

confidence: 93%

“…KORANSKY et al (1964) found that the a-, ß-, and y-isomers (lindane) of benzenehexachloride (BHC) activated liver microsomal enzymes. This activating effect persisted for different periods after single doses of each of the three isomers.…”

Section: B) Organochlorine Compoundsmentioning

confidence: 99%

Residue Reviews / Rückstands-Berichte

1967

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“…Long-term treatment with α-BHC, but not β- and γ-BHC, at high doses (500 or 1,000 ppm) has been revealed to induce hyperplastic nodules and liver carcinomas in rats and mice [59,60]. Furthermore, several toxicological studies found that α-, β-, and γ-BHC are potent inducers of hepatic monooxygenases in rats [61], in addition to causing liver enlargement [62]. …”

Section: Hormesis In Carcinogenicity Of Non-genotoxic Carcinogensmentioning

confidence: 99%

Oxidative Stress in the Carcinogenicity of Chemical Carcinogens

Kakehashi

Wei

Fukushima

et al. 2013

Cancers

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This review highlights several in vivo studies utilizing non-genotoxic and genotoxic chemical carcinogens, and the mechanisms of their high and low dose carcinogenicities with respect to formation of oxidative stress. Here, we survey the examples and discuss possible mechanisms of hormetic effects with cytochrome P450 inducers, such as phenobarbital, α-benzene hexachloride and 1,1-bis(p-chlorophenyl)-2,2,2-trichloroethane. Epigenetic processes differentially can be affected by agents that impinge on oxidative DNA damage, repair, apoptosis, cell proliferation, intracellular communication and cell signaling. Non-genotoxic carcinogens may target nuclear receptors and induce post-translational modifications at the protein level, thereby impacting on the stability or activity of key regulatory proteins, including oncoproteins and tumor suppressor proteins. We further discuss role of oxidative stress focusing on the low dose carcinogenicities of several genotoxic carcinogens such as a hepatocarcinogen contained in seared fish and meat, 2-amino-3,8-dimethylimidazo[4,5-f]quinoxaline, arsenic and its metabolites, and the kidney carcinogen potassium bromate.

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Aktivierung von Mikrosomenenzymen durch Hexachlorcyclohexan-Isomere. Ihr Einflu� auf die Scillirosidvergiftung der Ratte

Cited by 32 publications

References 11 publications

Hormesis in Carcinogenicity of Non-genotoxic Carcinogens

Hormesis in Carcinogenicity of Non-genotoxic Carcinogens

Residue Reviews / Rückstands-Berichte

Oxidative Stress in the Carcinogenicity of Chemical Carcinogens

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