Further examination of the effects of nitrosylation on Alternaria alternata mycotoxin mutagenicity in vitro.

摘要: Abstract Previously, Alternaria extract and metabolite mutagenicities ± nitrosylation were characterized using Ames Salmonella strains TA98 TA100, which are both reverted at GC sites. To examine other targets for mutation, the metabolites Altertoxin I (ATX I), Altenuene (ALT), Alternariol (AOH), monomethyl ether (AME), Tentoxin (TENT), Tenuazonic acid (TA) Radicinin (RAD) reexamined ± nitrosylation, strain TA97, sensitive to frameshift mutations a run of C's, as well TA102 TA104, by base pair AT sites more oxidative damage. ATX was also assessed mammalian mutagenicity Hprt gene locus in Chinese hamster V79 lung fibroblasts rat hepatoma H4IIE cells. When tested from 1 100 μg/plate without nitrosylation, mutagenic TA102 ± rat liver S9 activation weakly TA104 ± S9, demonstrating direct-acting mutagenicity. AOH directly TA102 ± S9 while AME TA104 + S9. Nitrosylation enhanced TA104 ± S9 but produced little change compared native I. However, nitrosylated generated potent mutagen C TA97 ± S9. While not either cells or cells, 5 10 μg/ml doubling 6-thioguanine resistant colonies 0.5 1 μg/ml becoming toxic higher concentrations. These results suggest I, induce sites, possibly through damage, with nitrosylation enhancing runs C's. Nitrosylated test systems.