EFFECTS OF VITAMIN-E-DEFICIENCY AND GLUTATHIONE DEPLETION ON STRESS PROTEIN HEME OXYGENASE-1 MESSENGER-RNA EXPRESSION IN RAT-LIVER AND KIDNEY

Heme oxygenase 1 (HO-1) is a stress protein and has been suggested to provide defense mechanisms against agents that may induce oxidative in jury. Vitamin E (VE) is considered to function as an important cellula r antioxidant. Rats were fed a VE-deficient (OE) or a VE-sufficient (1 0E) diet for 6 weeks and then were intraperitoneally administered buth ionine sulfoximine (BSO), a glutathione (GSH)-depleting reagent. Where as HO-1 mRNA levels were undetectable in untreated OE and 10E rat live rs, BSO administration induced HO-1 mRNA expression in both OE and 10E rat livers. High levels of HO-I mRNA expression were observed in part icular in BSO-treated OE rat livers. The time-course of changes in HO- 1 mRNA expression in OE rat liver after BSO administration showed that HO-1 mRNA expression was transiently induced at 2.5 hr after BSO trea tment, the earliest time examined. In addition, to determine whether V E deficiency and GSH depletion affect the expression of HO-1 mRNA in o ther tissues, we also examined the time-course of HO-1 mRNA expression in BSO-treated OE rat kidney. The expression pattern of HO-1 mRNA in the kidney was very similar to that in the liver, and the peak was als o observed at about 2.5 hr after BSO administration. Interestingly, hi stologic assessment of liver and kidney showed that VE deficiency and GSH depletion induced injury in the kidney, but not in the liver. (C) 1997 Elsevier Science Inc.