It. Mak et al., LOSS OF RED-BLOOD-CELL GLUTATHIONE DURING MG DEFICIENCY - PREVENTION BY VITAMIN-E, D-PROPRANOLOL, AND CHLOROQUINE, American journal of physiology. Cell physiology, 36(5), 1994, pp. 1366-1370
Mg deficiency results in loss of red blood cell glutathione and was th
ought to be due to decreased Mg-dependent synthesis. The effects of vi
tamin E, D-propranolol, and chloroquine on red blood cell glutathione
levels in Mg-deficient rats were examined. Feeding the rats a Mg-defic
ient diet for 3 wk resulted in an similar to 80% decrease in serum Mg
and a 55% loss of red blood cell glutathione; concomitantly, plasma th
iobarbituric acid reactive (TEAR) materials rose 240%, All three drug
treatments had no effect on the plasma Mg levels but significantly inh
ibited the rise in TEAR content and attenuated (60-80% effective) the
loss of glutathione. Red blood cell ghost membranes from the Mg-defici
ent rats also exhibited 2.3-fold higher TEAR content, which was attenu
ated by vitamin E treatment. With isolated red blood cells from Mg-suf
ficient rats, loss of glutathione could be induced by a chemical oxyra
dical system. Direct protective effects were afforded by cw-tocopherol
and D-propranolol but not by chloroquine. The data suggest that 1) th
e loss of glutathione during Mg deficiency was due to increased oxidat
ive degradation, 2) both vitamin E and D-propranolol protected by a me
mbrane antiperoxidative action, and 3) chloroquine probably protected
by diminishing prooxidant activity secondary to its inhibition of cyto
kine induction during Mg deficiency.