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We investigated melatonin effects on red blood cell (RBC) metabolism in an H 2 O 2-induced oxidative stress model. The study was carried out on three healthy adult donors by incubating RBCs in their own plasma at 37°C, or under the influence of 1 mM H 2 O 2 and 100 mM melatonin at different times (0, 1, 3 and 6 hours). We assessed incubation period, treatment, as well as interaction effects on oxidative stress markers, and adenine nucleotide and oxypurine levels. We found positive correlations between incubation times and hemolysis degree for each treatment. However, we did not observe any influence on RBC osmotic fragility and antioxidants tested. On the other hand, we found an increasing effect of incubation period on lipid peroxidation levels. Furthermore, oxidation induction regardless time more than doubled protein carbonyl groups in plasma but melatonin neutralized this H 2 O 2 effect. Unexpectedly, we did not find any relevant alterations on energy expenditure or adenylate nucleotide metabolism regarding to treatments or incubation periods investigated. The results obtained for markers of lipid and protein injury validated the auto incubation model, as well indicated a protection effect of melatonin. This effect along with its exceptional multiplicity actions reinforced the hypothesis of pharmacological use of melatonin in oxidative blood disorders.

This study investigated possible modulatory effects of melatonin treatment on red blood cell (RBC) metabolism in an auto incubation model. The study was carried out on six healthy donors (REF) and six sickle cell anemia patients by incubating RBCs in their own plasma at 37°C, during different times (0, 1, 3 and 6 hours). Furthermore, the sickle cells were incubated at the presence (tSCA) or absence (SCA) of 1 mM melatonin. We assessed incubation period and treatment effects on markers of membrane stability, hemolysis and antioxidant capacity, as well as metabolic enzymes and subproducts. We confirmed the well-known increased osmotic resistance of sickle cells. The hemolytic rate increased over time in all three groups, except in the tSCA group at 6 hours. Neither incubation nor treatment influenced AChE activity and plasma total antioxidant capacity (TAC). On the other hand, intra-erythrocyte TAC was higher in the REF after one hour of incubation. Moreover, melatonin treatment prevented NADPH cosumption and hemin formation, and it seemed to activate LDH. The protection effects of melatonin obtained indicate a promising use of melatonin as an antioxidant and alternative treatment for people with SCA.