Fatty acids, lipids, and cytochrome p-450 monooxygenase in hepatic microsomes of minks fed fish-based diets and exposed to Aroclor 1242.

Minks were fed different fish-based diets and exposed to 1 mg/d of the commercial polychlorinated biphenyl (PCB) mixture Aroclor 1242 for 4 wk (November-December 1995) or 21 wk (July-December 1998). In all the dietary groups, the PCBs increased hepatic phospholipid (PL) content. No significant increase was detected in hepatic triacylglycerols (TGs). In the minks fed the different fish diets, the PCBs caused qualitatively and quantitatively different changes in the microsomal fatty acids. In the minks that were fed a diet rich in fat and low in polyunsaturated fatty acids (PUFAs), the PCBs increased the percentage of oleic acid (18:1n-9, characteristic of the storage TGs) at the expense of n-3 PUFAs. This seemed to be due to inclusions of TGs in the membrane fragments and partly due to incorporation of TG-derived fatty acids into the membrane PLs. In addition, significant decrease of PUFAs was detected also in the hepatic TGs. The concomitant decrease in the concentrations of hepatic vitamin E suggested that lipid oxidation may also contribute to the decrease of the PUFAs. In the liver of the minks fed a low-fat but PUFA- and vitamin E-rich diet, the fatty acid changes due to the PCBs (the 21-wk exposure) remained small but the cytochrome P-450 system was significantly activated. In the minks fed Baltic herring (rich in organochlorines via the foodweb), the cytosolic glutathione S-transferase (GST) activity, levels of microsomal thiobarbituric acid-reactive substances (TBARS), and hepatic PLs were significantly elevated. In conclusion, in the mink the microsomal fatty acid changes were not directly connected with the ethoxyresorufin O-deethylase (EROD) activity or P-450 expression. Apparently, the PCBs produced definite fatty acid changes only in certain lipid matrices of tissue. In addition, a rich dietary supply of PUFAs and vitamin E may prevent these changes, even in a long-term subchronic exposure.