Effect of vitamins C and E on toxicity and mutagenicity of hexavalent chromium in rat and guinea pig

Chorvatovičová, Darina; Ginter, E; Kosinová, A; Zloch, Z

doi:10.1016/0165-7992(91)90104-c

Cited by 49 publications

(17 citation statements)

References 9 publications

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“…In studies with laboratory rodents, administration of radical scavengers simultaneously with or prior to administration of Cr(VI) salts reduced clastogenic potency, consistent with the oxygen radical mechanism of action (Chorvatovicova et al 1991(Chorvatovicova et al , 1993Sarkar, Sharma, and Talukder 1993). Results of in vitro mammalian cell studies showing reduction of Cr(VI)-induced DNA damage in the presence of a variety of oxygen radical scavengers, reducing agents, and metal chelators provide additional support for this mechanism (Pattison et al 2001;Cemeli et al 2003;O'Brien, Ceryak, and Patierno 2003).…”

Section: Mechanisms Of Genotoxicitymentioning

confidence: 66%

Mechanistic Insights from the NTP Studies of Chromium

et al. 2013

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Hexavalent chromium (Cr(VI)) is a contaminant of water and soil and is a human lung carcinogen. Trivalent chromium (Cr(III)), a proposed essential element, is ingested by humans in the diet and in dietary supplements such as chromium picolinate (CP). The National Toxicology Program (NTP) demonstrated that Cr(VI) is also carcinogenic in rodents when administered in drinking water as sodium dichromate dihydrate (SDD), inducing neoplasms of the oral cavity and small intestine in rats and mice, respectively. In contrast, there was no definitive evidence of toxicity or carcinogenicity following exposure to Cr(III) administered in feed as CP monohydrate (CPM). Cr(VI) readily enters cells via nonspecific anion channels, in contrast to Cr(III), which cannot easily pass through the cell membrane. Extracellular reduction of Cr(VI) to Cr(III), which occurs primarily in the stomach, is considered a mechanism of detoxification, while intracellular reduction is thought to be a mechanism of genotoxicity and carcinogenicity. Tissue distribution studies in additional groups of male rats and female mice demonstrated higher Cr concentrations in tissues following exposure to Cr(VI) compared to controls and Cr(III) exposure at a similar external dose, indicating that some of the Cr(VI) escaped gastric reduction and was distributed systemically. The multiple potential pathways of Cr-induced genotoxicity will be discussed.

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Section: Mechanisms Of Genotoxicitymentioning

confidence: 66%

Mechanistic Insights from the NTP Studies of Chromium

et al. 2013

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“…These highly reactive oxygen species can cause extensive tissue damage through reactions with all biological macromolecule, e.g., lipids, proteins and nucleic acids, leading to formation of oxidized substances, such as MDA, which is the product membrane lipid peroxidation (Halliwell & Gutteridge 1993). In animals, renal and chromosomal damage due to cisplatin, other heavy metals and doxorubicin-induced cardiomyopathy can be prevented by supplementation with high doses of antioxidants, such as selenium, vitamins C and E, without compromising the anti-tumour activity (Wang et al 1980;Fujita et al 1982;Ohkawa et al 1988;Chorvatovicova et al 1991;Whanger 1992;Jotti et al 1993). For instance, Ohkawa et al (1988) have demonstrated in mice that selenium co-administration allows higher doses of cisplatin with reduction of nephro-and hematological toxicity, resulting in a higher therapeutic index.…”

Section: Discussionmentioning

confidence: 99%

Chemopreventive effect of bilberry (Vaccinium myrtillus) against cisplatin-induced oxidative stress and DNA damage as shown by the comet assay in peripheral blood of rats

Pandır

Kara

2014

Biologia

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The aim of this study was to evaluate the chemopreventive effect of bilberry on cisplatin induced oxidative stress and DNA damage in rat blood. Twenty-one female Wistar-Albino rats were divided into three groups: group Iuntreated; group II -treated with cisplatin (single dose 7.5 mg/kg b.w.); and group III -treated with cisplatin (single dose 7.5 mg/kg b.w.) and bilberry (200 mg/kg b.w. for 10 days). Antioxidant enzyme systems including superoxide dismutase, catalase, glutathione peroxidase and the level of malondialdehyde (MDA) that might occur on erythrocytes have been determined and single cell gel electrophoresis (comet) was utilized to evaluate the DNA damage in lymphocytes. Treatment with cisplatin has increased the levels of MDA and decreased antioxidant enzymes in erythrocytes. Comet assay showed significantly higher values at dose of 7.5 mg/kg cisplatin as the result of oxidative DNA damage when compared to the control group. Cisplatin treatment with bilberry resulted in a highly significant (P < 0.05) decreased in the lymphocytes DNA when compared to the cisplatin group. Bilberry has been effective on antioxidant enzyme systems and MDA level and significantly decreased the comets. Our results indicate that bilberry is capable of preventing genotoxic and cytotoxic damage caused by cisplatin in peripheral blood cells in rats.

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“…Experimental data suggest that these antioxidants such as carotenoids, vitamin C and vitamin E can interact synergistically; they protect each other from degradation and/or promote their regeneration [197][198][199][200]. Low serum levels of Vitamin C in high risk population may contribute to the increased risk of chronic gastritis or gastric metaplasia, which are both precancerous lesions [201].…”

Section: Non-enzymatic Antioxidantsmentioning

confidence: 99%