H. Borba

Genotoxicity of nitrosated red wine and of the nitrosatable phenolic compounds present in wine: tyramine, quercetin and malvidine-3-glucoside.

Phenolic compounds and biogenic amines are known to be present in some foodstuffs which become directly genotoxic after nitrosation in vitro. Red wine has previously been shown to be genotoxic and this activity has been attributed mainly to flavonoids. Besides flavonoids, red wine contains a multiplicity of compounds, including biogenic amines. Using the Ames assay and the SOS chromotest, this study has shown that red wine and some of the nitrosatable molecules present in wine become directly genotoxic on nitrosation in vitro: these include the phenolic molecules tyramine, quercetin and malvidine-3-glucoside, whereas phenylethylamine and histamine were negative on nitrosation. Interestingly, quercetin had been predicted to be negative after nitrosation, using the CASE methodology. The concentrations of these three positive nitrosatable compounds in wine were determined by HPLC. Comparison of these concentrations and their respective levels of genotoxicity suggests that the genotoxicity after nitrosation is probably attributable to other molecules. It is also possible that synergistic effects may occur between various nitrosatable compounds in wine.

DNA Damage and Oxygen Species

Various genes are involved in cell protection against oxidative stress (e.g., SOD, catalase, GSH peroxidase) and some genes recognize and repair oxidative damage to DNA (both base and sugar damage). Yet, the nature and relative rates of the reactions involving active oxygen species make it difficult to ascertain, in each particular situation, what reactants may act as the predominant genotoxicant and what DNA repair mechanisms may ensue.

Evaluation of some biomonitoring markers in occupationally exposed populations to acrylonitrile

In the present work we studied acrylonitrile (AN) occupationally exposed populations and respective control individuals working in a Portuguese plant producing acrylic textile fibers. Three subgroups of individuals were considered: controls (C), workers of the continuous polymerization (CP) area, and workers of equipment maintenance (MM). Besides aiming to contribute to a better understanding of the hazardous exposure of man to AN, the study aimed to help validate and optimize the use of a combination of methods applied to human populations exposed to genotoxic compounds. Three main compartments related to the dose or effect of the hazardous compound were evaluated using various assessment methods: 1) internal dose (genotoxicity in urine, indicators of oxidative stress, induction of cytochromes P450); 2) biological effective dose (hemoglobin adducts); and 3) early biological effects (chromosomal aberrations, sister chromatid exchanges). Although concern with exposure to AN has long been the subject of numerous studies, they have been carried out essentially in animals and using in vitro systems. The significant differences (P < 0.01) found in the chromosomal aberrations of MM are in agreement with the highly significant levels of hemoglobin adducts described in another study performed in the same population. Hemoglobin adducts were also sensitive in detecting a hazardous exposure in the case of CP. The results obtained for the lipid peroxidation indicator used seem to confirm the AN capability of inducing lipid peroxidation in vivo. From the results available it seems that chromosomal aberrations as well as hemoglobin adducts are accurate and sensitive biomonitoring markers for AN exposure.