[Alcohol, iron and oxidative stress]

An oxidative stress has been reported to occur at the hepatic level after ethanol administration. We recently reported that such a stress is also apparent at the cerebellar level during acute ethanol intoxication in rats. Since low molecular weight iron chelates (LMW-Fe) are involved in the biosynthesis of aggressive prooxidant species we presently studied the influence of acute and chronic ethanol administration on hepatic and cerebellar total non-heme iron and LMW-Fe. The results show that an acute ethanol load (50 mmoles/kg b. wt.) administered (i.p.) to male Sprague-Dawley rats elicits altogether a decrease in the non-heme iron content of the serum and a highly significant increase in the hepatic and cerebellar non-heme iron concentration. The LMW-Fe content as well as the percentage of total non-heme iron represented by LMW-Fe are increased at the same time in the cytosolic fraction isolated from hepatic and cerebellar homogenates of the acutely ethanol-treated rats. The ethanol-induced disturbances in the non-heme iron content of liver and cerebellum can be prevented by the administration of allopurinol, which is known to reduce the severity of the oxidative stress observed in these tissues after an acute ethanol load. To study the effects of chronic ethanol administration, rats were given during 4 weeks a 10% (v/v) solution of ethanol in water as sole drinking fluid. The average daily ethanol consumption was 7-9 g. In such alcohol-fed rats the non-heme iron content was decreased by 31% in the serum whereas it was increased by 18% in the liver and by 30% in the cerebellum.(ABSTRACT TRUNCATED AT 250 WORDS)