Inhibition by fatty acids of direct mutagenicity of N-nitroso compounds.
Fatty acids inhibited the direct mutagenicity of N-nitroso compounds in Salmonella typhimurium TA1535, Escherichia coli WP2 and WPhcr-, and E. coli H/r30R (wild) and Hs30R (uvrA). This inhibitory activity was dependent on the concentration of fatty acids, and fatty acids with longer alkyl chain were more potent. Of the N-nitroso compounds tested, alpha-hydroxy nitrosamines underwent the strongest inhibitory effect. The rate of decomposition was not changed by addition of fatty acids. The partitioning property of the mutagens was altered but not to such a degree as to explain the amount of inhibition. No significant difference in alkylating activity of the N-nitroso compounds was observed in phosphate and acetate buffers. A stronger inhibition of mutagenicity by a butylating mutagen was detected in E. coli WP2 than in WP2hcr- and in E. coli H/r30R than in Hs30R, suggesting that excision repair was a possible mechanism of inhibition. The mutagenicity and cytotoxicity of alpha-hydroxy nitrosamines in Chinese hamster V79 cells were also inhibited by acetate.
Takeda
K
K
Kyoritsu College of Pharmacy, Tokyo, Japan.
Ukawa
S
S
Mochizuki
M
M
D000818:Animals; D006224:Cricetinae; D005227:Fatty Acids / Q000494:pharmacology*; D009153:Mutagens; D009603:Nitroso Compounds / Q000633:toxicity*; D012486:Salmonella typhimurium / Q000187:drug effects; D013329:Structure-Activity Relationship
D005227:Fatty Acids; D009153:Mutagens; D009603:Nitroso Compounds