Time and Dose-Dependent Effects of Dietary Cyclopropenoid Fatty Acids on the Mixed-Function Oxidase System of Rainbow Trout

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Aquatic Toxicology







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Rainbow trout (Salmo gairdneri) were fed diets containing various levels of cyclopropenoid fatty acids (CPFA's) and sampled at several time intervals to measure the effects on the mixed function oxidase (MFO) system. Feeding rainbow trout a diet containing 300 ppm CPFA's for 1 wk was sufficient to cause measurable changes in hepatic cytochrome P-450 content, microsomal protein content, NADPH—cytochrome creductase activity, and aryl hydrocarbon hydroxylase activity. After 3 wk, diets containing 50, 150 or 300 ppm CPFA's caused variable effects on mixed function oxidase (MFO) enzyme activities; however, diets containing 450 and 600 ppm CPFA's suppressed NADPH—cytochrome c reductase, ethoxycoumarin-O-deethylase, aryl hydrocarbon hydroxylase, p-nitroanisole-O-demethylase, epoxide hydrase, and glutathione transferase activities and decreased cytochrome P-450 and microsomal protein content compared to controls. The suppressive effects of dietary CPFA's on the trout MFO system is consistent with the decreased ability of liver from trout fed CPFA's to biotransform aflatoxin B1 (AFB1) to less active derivatives. The S20 liver fraction from trout fed diets containing CPFA's however, did not enhance the mutagenic activity of AFB1 using Salmonella typhinurium TA 98. The results indicate that dietary CPFA's in trout do not induce the cytochrome P-450 dependent microsomal MFO system which converts AFB1 to the active 2,3-oxide. The mechanism by which dietary CPFA's act as synergists with AFB1 seems to be through the post-initiation promotion of AFB1 formed lesions rather than through alteration of the MFO system or AFB1 metabolism.


Originally published by Elsevier. Publisher's PDF available through remote link.