Dependence of the rate of metabolism of Benzo[a] Pyrene on the fatty acid composition of the liver endoplasmic reticulum and on the dietary lipids

Abstract

The effect of dietary lipid content on the fatty acid composition of the liver endoplasmic reticulum and the effect of the fatty acid composition on the oxidative metabolism of Benzo (a) Pyrene (BP) in the liver endoplasmic reticulum were studied in rats. The rate of oxidative metabolism of BP was found to be markedly dependent on the percentage of polyunsaturated fatty acids incorporated into the membrane of the endoplasmic reticulum. Diets containing 10% lard or 10% corn oil caused the incorporation of 10.3% and 25.1% linoleicacid (C 18:2 ) and oxidation rates of 68.3 and 113.8 nmol 3-hydroxybenzo (a) pyrene/30 min/g liver, respectively. Diets containing 10% herring oil caused incorporation of only 5.1 % C 18:2 but also 27.2% ω3 unsaturated fatty acids, including 8.7% eicosapentaenoic acid (C 20:5 ) and 17.0% docosahexaenoic acid (C 22:6 ) and caused a high oxidation rate (145.8 nmol) 3-hydroxybenzo (a) pyrene/30 min/g liver.Phenobarbitone (100 mg/kg) and 20-methylcholanthrene (20 mg/kg) strongly enhanced the oxidation rate of BP in groups of rats fed a herring oil diet and induction was much greater in the group fed an irradiated diet than in the group fed an untreated herring oil diet. Irradiation with 400 krad caused destruction of the major proportion of the polyunsaturated fatty acids in herring oil, incorporation of a smaller quantity of ω3 unsaturated acids into the endoplasmic reticulum, and a decrease in the rate of oxidation to 122.5 nmol 3-hydroxybenzo (a) pyrene/30 min/g liver.The antioxidant 2,6-di-tert-butyl-4 methylphenol, BHT, (0.01 %) added to irradiated herring oil diets strongly reduced the inductive effect of phenobarbitone. This effect may therefore be caused by the presence of lipid peroxides in the irradiated diet.It is concluded that dietary C 18:2 is an important factor in the regulation of the rate of oxidative metabolism of BP in the liver endoplasmic reticulum, but C 18:2 may be effectively replaced by dietary C 20:5 and C 22:6 . Oxidation of BP is regulated by changes in the fatty acid composition of the membranes of the liver endoplasmic reticulum.

Liver Microsomal Mixed-Function Oxidases in Response to Polyunsaturated/Saturated and n-6/n-3 Fatty Acid Ratios of Dietary Lipids in Rats

“…It has been reported so far that dietary fish oils rich in n-3 fatty acids, but a m ixture of n-3 and n-6 fatty acids, increase the activities of liver microsomal MFO system with [30][31][32][33] or without [7,9,11,20,34] inducing agents such as PB and dimethylbenz(a)anthracene as com pared with other edible oils rich in LA. The present findings confirmed and extended such results.…”

“…It has generally been shown so far that saturated fats such as beef tallow, coconut oil and palm oil decrease the MFO activity and conversely polyunsaturated fats increase the activity [6][7][8][9][10][11][12], As shown in fig ure 1 and tables 2 and 3, when the MFOs were not induced by PB, the highest P/S ratio tended to increase the MFO activities, and the degree of unsaturation of microsomal mem brane fatty acids increased with increasing the dietary P/S ratio as assessed by the double bond index (an indicator of membrane fluidi ty). This observation is consistent with the hitherto obtained results using different types of dietary fats which are varied in both the P/S and n-6/n-3 ratios of component fatty acids [6,7,[9][10][11]20], That is, both the n-6 and n-3 PUFAs play an important role in increasing the MFO activities by elevating the degree of unsaturation of microsomal membrane fatty acids. And, n-6 fatty acids such as LA and AA in liver microsomes are interchanged effi ciently by n-3 fatty acids such as EPA, DPA and DHA in order to support a basal unin duced activity of the membrane-bound MFO system.…”