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M Castegnaro

Publications and source records attributed to M Castegnaro.

110 records · Page 7Linked to original sources

International N-nitroso compounds check sample programme: report on the performance in the second study dedicated to their determination in beer and malt.

The second check sample survey for the determination of N-nitrosamines in beer and malt has been initiated. Each laboratory received four samples: two beer, from the same batch, spiked respectively with 0.5 microgram/l N-nitrosodimethylamine (NDMA) and 4 micrograms/l NDMA plus 30 micrograms/l N-nitrosoproline (NPRO) and two naturally contaminated malts. Sixteen laboratories sent their results and two apologized in view of analytical problems. Results from this have been statistically evaluated. Comparison to those from the previous study demonstrated a distinct improvement in the results from the analysis of NDMA in beer and malt. Little has been achieved for the other two common contaminants of beer and malt, N-nitrosopyrrolidine (NPYR) and NPRO. For this latter compound in beer, however, some hope came from the data produced by the method of Sen et al. (1983), but the number of results is insufficient to allow firm conclusions to be drawn.

Beer↗

Interstrain comparison of hepatic and renal microsomal carcinogen metabolism and liver S9-mediated mutagenicity in DA and Lewis rats phenotyped as poor and extensive metabolizers of debrisoquine.

Lewis (extensive metabolizers) and DA (poor metabolizers) rat strains show genetic polymorphism for the gene regulating debrisoquine 4-hydroxylation in a manner analogous to human drug polymorphism and show also a different toxicological response to aflatoxin B1. In order to investigate the underlying mechanism(s) of the different drug-metabolizing capacities, the in vitro metabolism and liver S9-mediated mutagenicity of several drugs and carcinogens were studied in female Lewis and DA rat strains, using untreated, 3-methylcholanthrene-treated, and phenobarbital-treated animals. S9-mediated mutagenicity of aflatoxin B1 and hepatic and renal ochratoxin A 4-hydroxylase activity were much lower in DA rats; however, the activity of a number of other hepatic and renal drug-metabolizing enzymes did not show any interstrain difference. Slight strain differences were found in the inducibility of several hepatic drug-metabolizing enzymes, except for ochratoxin A 4-hydroxylase activity; the latter was inducible only by 3-methylcholanthrene in the DA strain and appeared to be linked genetically with other Ah locus-associated monooxygenases. Our data suggest that ochratoxin A 4-hydroxylase activity, which is low in the DA strain, is catalyzed by a cytochrome P-450 isozyme different from that responsible for debrisoquine 4-hydroxylation. Our results provide some insight into why the two metabolic oxidation phenotypes show different susceptibility to cancer induction and to the toxicity of certain environmental carcinogens, such as aflatoxin B1 and ochratoxin A.

2-Acetylaminofluorene↗