Kudo N, Nakagawa Y, Waku K, Kawashima Y, Kozuka H
Faculty of Pharmaceutical Sciences, Teikyo University, Kanagawa, Japan.
Toxicology. 1991;68(2):133-42. doi: 10.1016/0300-483x(91)90016-t.
Rats were fed a fat-free diet that contained zinc (50 ppm; ZA rats) or a fat-free diet without zinc (less than 2 ppm; ZD rats) for 16 days. Some rats in these two groups were injected subcutaneously with cadmium (Cd) at a dose of 0.01 mmol/kg body weight 48 h before they were killed. The treatment of ZD rats with Cd reduced the activity of liver microsomal stearoyl-CoA desaturase by 90% without any changes in the activity of NADH-cytochrome b5 reductase or in the microsomal level of cytochrome b5 whereas the activity of stearoyl-CoA desaturase was reduced by only 35% by the treatment of ZA rats with Cd. Exposure of ZD rats to Cd decreased the proportions of 18:1 (n-9) and 20:3 (n-9) in the major phospholipids of the liver, whereas the ZA rats showed few changes in fatty acid composition when they were treated with Cd. Although the changes in fatty acid composition were most marked in phosphatidylcholine among the various phospholipids, the activity of microsomal l-acylglycerophosphocholine (1-acyl GPC) acyltransferase was not affected by treatment with Cd. These results suggest that zinc is essential for the protection of hepatic stearoyl-CoA desaturase from challenges by Cd and that delta 9 desaturase plays a crucial role in the control of the acyl composition of hepatic phospholipids.