J. Biochem, 1990, Vol. 107, No. 5 689-693
© 1990 Japanese Biochemical Society
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Phospholipid Hydroperoxide Accumulation in Liver of Rats Intoxicated with Carbon Tetrachloride and Its Inhibition by Dietary 
-Tocopherol
*Department of Food Chemistry, Faculty of Agriculture, Tohoku University Aoba-ku, Sendai, Miyagi 981;
**Department of Food and Nutrition, Kohriyama Women's College Kohriyama, Fukushima 963
1 To whom correspondence should be addressed.
The formation and accumulation of phospholipid hydroperoxides, especially of phos-phatidylcholine hydroperoxide (PCOOH), a primary peroxidation product of phos-phatidylcholine (PC), in livers of carbon tetrachloride-intoxicated rats was investigated. PCOOH in liver and blood plasma was measured by a chemiluminescence-high-perform-ance liquid chromatography procedure originally developed by Miyazawa et al. (AnaL Lett, 20, 915, 1987; Free Radical Biol Med. 7, 209, 1989). Male Sprague-Dawley rats (120 g body wt., 5 weeks of age) were used in the experiments. The amount of PCOOH in the liver of control rats (CC14-untreated) was 160±20pmol/100mg protein (mean±SD) and the PCOOH/PC molar ratio was l.l±0.1Xl05, In CC14 (0.1 ml/100 g body wt.)-dosed rats, the liver PCOOH was 289±65pmol/100mg protein (PCOOH/PC=2.4±0.4xlO–5), 764±271 pmol/lOOmg protein (PCOOH/PC=5.2±1.7X10–5), and 856±165pmol/100mg protein (PCOOH/PC=6.0±0.8x10–5) at 6h, 24 h, and 1 week after the dose, respectively. Under such conditions, the liver phosphatidylethanolamine hydroperoxide (PEOOH) level was not altered and the concentration was less than 100 pmol/100 mg protein even after the dose. The increments of liver PCOOH were suppressed 56% by the oral supplementation of DL-a-tocopherol (5 mg/100 g body wt./day) for a week before CC14 administration. A relatively larger amount of PEOOH was found after stimulation of PC hydroperoxidation in the liver of rats with a large amount of CC14 (0.25 ml/100 g body wt.) rather than with the small amount of CC14 (0.1 ml/100 g body wt.). On the other hand, the amount of plasma PCOOH was less than 10 nM in the control rats and also in the CC14 (0.1 ml/100 g body wt.)-treated rats at 6 and 24 h after the dose, but 1 week after the dose, plasma PCOOH showed a large increase to 135 ±9 nM. The results indicate that PC is the most susceptible lipid class to lipid hydroperoxidation in vivo, and dietary a-tocopherol inhibits the PC hydroperoxidation.
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