Mak I T, Stafford R, Weglicki W B
Department of Physiology, George Washington University Medical Center, Washington, District of Columbia 20037.
Am J Physiol. 1994 Nov;267(5 Pt 1):C1366-70. doi: 10.1152/ajpcell.1994.267.5.C1366.
Mg deficiency results in loss of red blood cell glutathione and was thought to be due to decreased Mg-dependent synthesis. The effects of vitamin E, D-propranolol, and chloroquine on red blood cell glutathione levels in Mg-deficient rats were examined. Feeding the rats a Mg-deficient diet for 3 wk resulted in an approximately 80% decrease in serum Mg and a 55% loss of red blood cell glutathione; concomitantly, plasma thiobarbituric acid reactive (TBAR) materials rose 240%. All three drug treatments had no effect on the plasma Mg levels but significantly inhibited the rise in TBAR content and attenuated (60-80% effective) the loss of glutathione. Red blood cell ghost membranes from the Mg-deficient rats also exhibited 2.3-fold higher TBAR content, which was attenuated by vitamin E treatment. With isolated red blood cells from Mg-sufficient rats, loss of glutathione could be induced by a chemical oxyradical system. Direct protective effects were afforded by alpha-tocopherol and D-propranolol but not by chloroquine. The data suggest that 1) the loss of glutathione during Mg deficiency was due to increased oxidative degradation, 2) both vitamin E and D-propranolol protected by a membrane antiperoxidative action, and 3) chloroquine probably protected by diminishing prooxidant activity secondary to its inhibition of cytokine induction during Mg deficiency.
镁缺乏会导致红细胞谷胱甘肽丢失，过去认为这是由于镁依赖性合成减少所致。研究了维生素E、D-普萘洛尔和氯喹对缺镁大鼠红细胞谷胱甘肽水平的影响。给大鼠喂食缺镁饮食3周后，血清镁水平下降约80%，红细胞谷胱甘肽损失55%；与此同时，血浆硫代巴比妥酸反应性（TBAR）物质增加了240%。所有三种药物治疗对血浆镁水平均无影响，但显著抑制了TBAR含量的升高，并减轻了（有效率60 - 80%）谷胱甘肽的损失。缺镁大鼠的红细胞血影膜的TBAR含量也高出2.3倍，维生素E治疗可使其降低。对于镁充足大鼠的分离红细胞，化学氧自由基系统可诱导谷胱甘肽丢失。α-生育酚和D-普萘洛尔具有直接保护作用，而氯喹则没有。数据表明：1）镁缺乏期间谷胱甘肽的丢失是由于氧化降解增加所致；2）维生素E和D-普萘洛尔均通过膜抗过氧化作用起到保护作用；3）氯喹可能是通过减少缺镁期间细胞因子诱导继发的促氧化活性而起到保护作用。
