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)

During the preparation of spheroplasts, adenine phosphoribosyltransferase (EC 2.4.2.7) and hypoxanthine phosphoribosyltransferase (EC 2.4.2.8) were released in parallel with cytidine deaminase (EC 3.5.4.5) and uridine phosphorylase (EC 2.4.2.3), which, on other evidence, are considered to be located intracellularly. The two phosphoribosyltransferases and uridine phosphorylase were not significantly associated with purified membrane fractions as was purine nucleoside phosphorylase (EC 2.4.2.1). The effects of the poorly permeable enzyme-inactivating reagents, 4-diazoniumbenzenesulphonate, 7-diazonium-1,3-naphthalene-disulphonate and 2,4,6-trinitrobenzenesulphonate, on Escherichia coli indicate that all the above-mentioned enzymes and also the xanthine-guanine phosphoribosyltransferase [Miller, Ramsey, Krenitsky & Elion (1972) Biochemistry 11, 4723--4731] are located intracellularly.
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PMID:The location of purine phosphoribosyltransferase activities in Escherichia coli. 36 72

The genotoxic risks from exposure to polycyclic aromatic hydrocarbons (PAH) have long been recognized. Less well understood are the potential genotoxic risks of the atmospheric reaction products of this class of compounds. In this investigation, we have utilized several human cell genotoxicity assays to evaluate naphthalene, phenanthrene, and their atmospheric reaction products 1-nitronaphthalene, 2-nitronaphthalene, 1-hydroxy-2-nitronaphthalene, 2-hydroxy-1-nitronaphthalene, 1,4-naphthoquinone and 2-nitrodibenzopyranone. In addition, reaction products of naphthalene were generated in a 6700-1 Teflon environmental chamber, collected on a solid adsorbent, extracted and fractionated by normal-phase HPLC. Individual fractions were then analyzed using GC-MS, and tested for genotoxicity. Genotoxicity was determined using the human B-lymphoblastoid cell line, MCL-5, which expresses several transfected P450 and epoxide hydrolase genes. Mutagenicity was evaluated at both the heterozygous tk locus and the hemizygous hprt locus, permitting detection of both intragenic and chromosomal scale mutational events. Test compounds were also screened using the CREST modified micronucleus assay. Genotoxicity results indicate that 2-nitronaphthalene and 2-nitrodibenzopyranone possess greater mutagenic potency than their parent compounds, and interestingly, both compounds induced significant increases in mutation frequency at tk but not hprt. These results suggest a mechanistic difference in human cell response as compared to bacteria, where both compounds were previously shown to induce point mutations in the Salmonella reversion assay. The genotoxicity of 2-nitronaphthalene and 2-nitrodibenzopyranone in human cells, together with their high concentrations in ambient air relative to nitro-PAH directly emitted from combustion sources, emphasizes the need to consider atmospheric reaction products of PAH in genotoxicity assessments.
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PMID:Genotoxicity induced in human lymphoblasts by atmospheric reaction products of naphthalene and phenanthrene. 935 59

We have investigated the mutagenicity of oxidative DNA damage induced in V79 Chinese hamster lung fibroblast, and measured 8-hydroxydeoxyguanosine (8OHdG) levels as an indicator of this damage. A hydroxyl radical generator, N,N'-bis(2-hydroxyperoxy-2-methoxyethyl)-1,4,5,8-naphthalene-tetra -carboxylic-diimide (NP-III), induced 8OHdG in V79 upon irradiation with 366 nm ultraviolet light (UV) for 15 min. 8OHdG was determined by HPLC with electrochemical detection after anaerobic sample processing. The 8OHdG level in the cells treated without NP-III was 0.49 per 10(5) dG, whereas levels in the cells treated with 5, 10 or 20 microM NP-III and UV irradiation were 1.84, 4.06 or 6.95 per 10(5) dG, respectively. The 8OHdG induced by 20 microM NP-III with UV irradiation decreased rapidly, and the half-life of the induced 8OHdG was approximately 6 h. NP-III with UV irradiation also induced DNA strand breaks in all cells uniformly, as determined by single cell gel assay. Mutant frequencies at the hypoxanthine-guanine phosphoribosyltransferase (hprt) locus in V79 were determined as the number of 6-thioguanine-resistant cells per 10(6) cells. Mutant frequency of the cells without NP-III was 8.0, and frequencies of the cells treated with 5, 10 or 20 microM NP-III and UV irradiation were 14.9, 20.6 or 24.7 respectively. Treatment with 20 microM NP-III and UV irradiation decreased the cell number, determined 3 days after the treatment, to 20.8%. These findings indicate that acutely induced oxidative DNA damage including mutagenic 8OHdG is only weakly mutagenic in V79.
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PMID:Mutagenicity of oxidative DNA damage in Chinese hamster V79 cells. 939 1