MELATONIN REDUCES OXIDATIVE DAMAGE INDUCED BY ALUMINIUM IN RAT KIDNEY. Toxicology letters [Toxicol Lett] Journal article

We evaluated the effect of melatonin (Mel), in male Wistar rats which received aluminium (Al) lactate for 12 weeks (0.57mg Al/100g body weight (bw), i.p. three times per week). Moreover rats received Mel (10mg/kg bw i.p. five days/ weeks) for 12 weeks. At the end of the treatment water and sodium balances were studied, and nephrogenic cAMP was also measured. Urinary osmolality were measured after administration of desmopressin (vasopressin agonist) to asses concentrating capacity. Oxidative stress in renal tissue and Na(+)-K(+)ATPase and gamma-glutamyl transferase (GGT) activities in whole plasma membrane were determined. Sodium and water balance were impaired by Al. We found decreased urinary concentrating ability and nephrogenic cAMP excretion. Al increased the Na(+)-K(+)ATPase activity, and serum aldosterone concentration. Mel normalized serum aldosterone level, the Na(+)-K(+)ATPase activity and potassium urinary without improve water and sodium excretion. Mel treatment did not improve the impaired urinary concentrating ability. Al reduced the GGT activity, an effect that persists in Al + Mel. Al exposure promoted oxidative stress with an increased of LPO, a decreased of GSH and GSH-Px and CAT activities. Mel markedly attenuated oxidative stress produced by Al. This may be the results for the higher efficacy of melatonin in scavenging various free radicals and also because of its ability in stimulating the antioxidant enzymes. However, it only reduced some alterations in the renal functions particularly related to the water and sodium excretion, which would be independent of the increase production of reactive oxygen substances.

Toxicology letters [Toxicol Lett]