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Effect of ten thiocompounds on rat liver DNA damage induced by a small dose of N-nitrosodimethylamine (1992)

Brambilla, Giovanni ; Carlo, Pia ; Finollo, Renata

Springer

Archives of toxicology 66 (1992), S. 286-290

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ISSN: 1432-0738

Keywords: N-Nitrosodimethylamine ; Thiocompounds ; Rat liver DNA damage ; Viscometric analysis of DNA fragmentation

Source: Springer Online Journal Archives 1860-2000

Topics: Medicine

Notes: Abstract The use in a chemoprevention study of high doses of the genotoxic agent might result in erroneous information because of possible nonlinearity of pharmacokinetic processes and toxicity-induced derangement of physiological defense mechanisms. According to these premises ten thiocompounds, potentially active as inhibitors of metabolic activation and/or scavengers, were examined for their capability of reducing the frequency of liver DNA lesions induced by a very small dose of N-nitrosodimethylamine (NDMA). This was accomplished by means of a viscometric technique previously found suitable to detect a minimal amount of DNA fragmentation. Rats were injected i.p. or i. v. with 1 mmol/kg of thiocompound, 0.2 mg/kg NDMA given by gavage 1 h afterwards, and killed for DNA damage assessment 14 h later. Statistically significant changes of viscometric parameters, which are considered indicative of a protective activity, were produced by disulfiram (DSF), and to a lower extent by diethyldithiocarbamate (DEDTC). Any modification of NDMA-induced DNA damage was absent in rats pretreated with glutathione reduced form (GSH) and dimethyl sulfoxide (DMSO). Allyl disulfide (ADS), L-cysteine (CYS), N-acetylcysteine (NAC), α-mercaptopropionylglycine (MPG), ethylxanthic acid (PEX), and 2-mercaptoethane sulfonic acid (MESNA) increased in various degree the frequency of DNA-strand breaks. In subsequent experiments the protective activity of DSF was found to be dose-related, dependent on the time of administration, and greater by oral route. Taken as a whole, these results suggest that several putative anticarcinogens might be ineffective against the DNA-damage produced by the low doses encountered in human exposure.

Type of Medium: Electronic Resource

URL: http://dx.doi.org/10.1007/BF02307175

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DNA-damaging activity of biotic and xenobiotic aldehydes in chinese hamster ovary cells (1984)

Marinari, Umberto M. ; Ferro, Margherita ; Bassi, Anna Maria ; [et al.]

New York, NY [u.a.] : Wiley-Blackwell

Cell Biochemistry and Function 2 (1984), S. 243-248

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ISSN: 0263-6484

Keywords: Nucleic acids ; aldehydes ; lipid peroxidation ; DNA cross-links ; DNA single strand breaks ; cultured mammalian cells ; Chemistry ; Biochemistry and Biotechnology

Source: Wiley InterScience Backfile Collection 1832-2000

Topics: Biology , Medicine

Notes: Alkaline elution was employed to study DNA damage in CHO-Kl cells treated with a series of biotic and xenobiotic aldehydes. DNA cross-linking was measured in terms of the reduction in the effect of methyl methanesulphonate on the kinetics of DNA elution and was observed in cells treated with formaldehyde, acetaldehyde, methylglyoxal and malonaldehyde. Propionaldehyde, valeraldehyde, hexanal and 4-hydroxynonenal produced DNA single-strand breaks, or lesions which were converted to breaks in alkali. Both types of DNA damage occurred in cells exposed to malealdehyde. These findings support the hypothesis of a carcinogenic effect of the aldehydic products (malonaldehyde, methylglyoxal, propionaldehyde, hexanal, 4-hydroxynonenal) released in biomembranes during lipid peroxidation.

Additional Material: 1 Ill.