ALLOPURINOL, AN INHIBITOR OF XANTHINE-OXIDASE, REDUCES URIC-ACID LEVELS AND MODIFIES THE SIGNS ASSOCIATED WITH COPPER DEFICIENCY IN RATS FED FRUCTOSE

This study was designed to focus on the potential stress that xanthine oxidase could produce in copper-deficient rats fed fructose. Fructose consumption results in an excess production of uric acid due to an in creased degradation of nucleotides. The enzyme xanthine oxidase cataly zes the oxidation of both hypoxanthine and xanthine. During the oxidat ion process free radicals are generated, which in turn, induce lipid p eroxidation and premature death. Allopurinol-a competitive inhibitor o f xanthine oxidase-could alleviate the combined effects of fructose fe eding and copper deficiency. Twenty-five male rats were fed for 4 week s from weaning a copper deficient or adequate diet containing fructose . Twelve rats were given a daily oral dose of 5 mg allopurinol/100 g b .wt. Two copper-deficient rats that were not treated with allopurinol died prematurely during the fourth week of the study. No mortality occ urred in the group of copper-deficient rats that had been treated with allopurinol. Anemia was alleviated by allopurinol, which in turn, cou ld be responsible for improved growth rate. Allopurinol was effective in inhibiting xanthine oxidase activity in vivo as measured by the dra matic reduction of uric acid production. Lipid peroxidation, however, was not affected by allopurinol. It is concluded that the beneficial e ffects of allopurinol in copper deficiency do not appear to be related to prevention of oxygen radicals, but rather, to the protection again st the catabolic destruction of purines, which in turn, increases nucl eotide pool.