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)

We measured the frequency of mutant (MF) lymphocytes at the hprt locus in a population of 43 coke-oven workers exposed to PAH and in a group of 26 non-exposed workers. A non-significant increase in MF in the exposed group (19.0 +/- 16.3) compared to the non-exposed group (15.8 +/- 14.6) was observed. Moreover, when we considered smoking habits for the overall population, the MF values were higher, although not significantly, in smokers than in non-smokers. For some T-cell mutant clone structural alterations, splicing and coding errors were detected by PCR-based methods. We analysed 161 HPRT- clones, derived from exposed and non-exposed workers by multiplex-PCR and 56 HPRT- clones by reverse transcriptase-PCR. Overall, the percentages of the different types of gene alterations were similar in exposed and non-exposed subjects. Only the frequency of splice mutations in mutant clones derived from coke-oven workers was higher (22%) than in non-exposed donors (11%).
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PMID:Determination of HPRT mutant frequency and molecular analysis of T-lymphocyte mutants derived from coke-oven workers. 953 72

Sediments are the sink for particle-sorbed contaminants in aquatic systems and can serve as a reservoir of toxic contaminants that continually threaten the health and viability of aquatic biota. This work is a comprehensive review of published studies that investigated the genotoxicity of sediments in rivers, lakes and marine habitats. The Salmonella mutagenicity test is the most frequently used assay and accounts for 41.1% of the available data. The Salmonella data revealed mutagenic potency values for sediment extracts (in revertants per gram dry weight) that spans over seven orders of magnitude from not detectable to highly potent (10(5) rev/g). Analyses of the Salmonella data (n=510) showed significant differences between rural, urban/industrial, and heavily contaminated (e.g., dump) sites assessed using TA98 and TA100 with S9 activation. Additional analyses showed a significant positive correlation between Salmonella mutagenic potency (TA98 and TA100 with S9) and PAH contamination (r2=0.19-0.68). The second and third most commonly used assays for the analysis of sediments and sediment extracts are the SOS Chromotest (9.2%) and the Mutatox assays (7.8%), respectively. These assays are frequently used for rapid initial screening of collected samples. A variety of other in vitro endpoints employing cultured fish and mammalian cells have been used to investigate sediment genotoxic activity. Endpoints investigated include sister chromatid exchange frequency, micronucleus frequency, chromosome aberration frequency, gene mutation at tk and hprt loci, unscheduled DNA synthesis, DNA adduct frequency, and DNA strand break frequency. More complex in vivo assays have documented a wide range of effects including neoplasms and preneoplastic lesions in fish and invertebrate exposed ex situ. Although costly and time consuming, these assays have provided definitive evidence linking sediment contamination and a variety of genotoxic and carcinogenic effects observed in situ.
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PMID:The mutagenic hazards of aquatic sediments: a review. 1557 85

The present review is based on findings from 178 publications retrieved through an extensive search of the MedLine/PubMed database for a 25 years time period (1980-2004) and 10 manually identified papers. Among the cytogenetic biomarkers that are frequently used in field studies, chromosome aberrations (CA) and micronuclei (MN) but not sister chromatid exchanges (SCE) were found consistently increased in children exposed to environmental pollutants. Meta-analysis of the studies reporting SCE in cord blood showed similar levels of SCE in exposed and in non-exposed newborns. Exposure to airborne pollutants, soil and drinking water contaminants, mostly increased CA and, to a lesser extent, MN levels in children. The effect of exposure to airborne urban pollutants was consistently reported by field studies measuring DNA, albumin and hemoglobin adducts. Prenatal (in utero) and postnatal exposure (environmental tobacco smoke, ETS) to tobacco smoke compounds were associated with increased frequencies of DNA and hemoglobin adducts and CA. The limited number of field studies measuring DNA fragmentation (Comet assay), hypoxanthine-guanine phosphoribosyltransferase (HPRT) and the glycophorinA (GPA) mutation frequency in environmentally exposed children precluded a meaningful evaluation of the usefulness of these assays. Meta-analyses performed in children exposed to ETS and in newborns exposed in utero to their mothers' smoke showed 1.3 and 7 times higher levels of hemoglobin adducts compared to referent subjects, respectively. These increases are consistent with the epidemiological evidence of higher lung cancer risks reported in adults who had never smoked and were exposed to ETS during childhood and with 7-15 times higher lung cancer risks reported in smokers than in non-smokers. Higher levels of PAH-DNA adducts were found in fetal than in maternal tissue, suggesting a specific susceptibility of the fetus to this class of ubiquitous environmental pollutants. According to these findings, future research and biomonitoring programs on children would greatly benefit from the inclusion of selected biomarkers that could provide biologically based evidence for the identification of intervention priorities in environmental health.
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PMID:Children's exposure to environmental pollutants and biomarkers of genetic damage. II. Results of a comprehensive literature search and meta-analysis. 1602 31