Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00492 (hypoxanthine-guanine phosphoribosyltransferase)
 2,385 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mutagenesis of several insoluble nickel compounds--crystalline nickel sulfide NiS, nickel subsulfide Ni3S2, nickel oxides (black and green) and soluble NiCl2 was studied in three Chinese hamster cell lines--at the hprt gene of the well-defined V79 cell line, and at gpt in two transgenic derivative cell lines G12 and G10. The transgenic cell line G12 responded very strongly to the insoluble Ni compounds, such that the gpt mutagenesis was at least 20 times higher than the spontaneous mutagenesis and in some experiments was even higher. In contrast the response of the G10 cells was much lower--the mutant frequencies only increased 2-3 times over the controls. In V79 cells, NiS and NiO (black) did not induce a mutagenic response at hprt. Soluble NiCl2 also exhibited no mutagenic activity in V79 cells and induced considerably lower activity than the insoluble compounds in the transgenic G12 cells. Following vitamin E pretreatment of G12 cells for 24 h prior to nickel exposure, increased cell survival was observed for several insoluble Ni compounds whereas vitamin E had no effect on NiCl2 cytotoxicity. With vitamin E pretreatment, significantly lower mutagenic responses in G12 cells were also noted for some insoluble Ni compounds, while no such effect was observed for NiCl2.
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PMID:Mutagenic responses of nickel oxides and nickel sulfides in Chinese hamster V79 cell lines at the xanthine-guanine phosphoribosyl transferase locus. 768 71

Hepatocytes freshly isolated from male Wistar rats fed a common diet or a vitamin A- or vitamin E-supplemented diet (each for 21, 28, or 41 days) were assayed for sensitivity to DNA breakage and cytogenetic changes induced by carcinogens. Different indirectly acting carcinogens were assayed. N-nitrosomorpholine (NMOR) was the only agent that induced DNA breaks, chromosomal aberrations, and micronuclei in all experiments. Benzo[a]pyrene (B[a]p) and dimethyldibenzo [c,g]carbazole (diMeDBC) induced only DNA breaks in all experiments. Occasionally, B[a]P induced chromosomal aberrations and micronuclei, and diMeDBC induced micronuclei, but not chromosomal aberrations. These results demonstrated that the tested carcinogens assayed at concentrations highly effective in a hypoxanthine phosphoribosyltransferase/V79 system significantly increased DNA damage, while cytogenetic changes were less frequent. In hepatocytes from rats fed vitamin A, a reduction in the severity of all three end points was observed after NMOR treatment. After B[a]P treatment, we found a reduction in DNA breaks and chromosomal aberrations; after treatment with diMeDBC, we observed a reduction in DNA breaks. Treatment with vitamin E was less effective: it reduced DNA strand breaks induced by B[a]P and partially reduced those induced by diMeDBC and NMOR and the level of micronuclei induced by NMOR and B[a]P. Both vitamins reduced the level of DNA strand breaks induced by the oxidative effect of a visible light-excited photosensitizer.
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PMID:Effect of dietary intake of vitamin A or E on the level of DNA damage, chromosomal aberrations, and micronuclei induced in freshly isolated rat hepatocytes by different carcinogens. 1223 43