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Backgrounds: Delta-aminolevulinic acid (ALA) is a heme precursor that accumulates in acute intermittent porphyria (AIP) due to enzymatic deficiencies in the heme biosynthetic pathway, its accumulation has been associated with several symptoms because it works as an endogenous source of reactive oxygen species, which can exert oxidative damage to cell structures. The present work was designed to examine the ability of melatonin, a well known antioxidant and a free radical scavenger secreted from the pineal gland, to revert ALA-promoted damage in brain, liver and kidney of rats. Results: The present data demonstrated that chronically ALA-treated rats (40 mg / kg body wt day after day for 14 days) exhibited very highly significant increases in malondialdehyde (MDA) and protein carbonyl (PC) whereas the level of glutathione (GSH) was significantly diminished in the tissue homogenates of all tested organs (brain, kidney & liver). Among antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GSH-Rd), glutathione-S-transferase (GST) activities were significantly diminished by ALA treatment. Intraperitoneal injection of melatonin (10 mg / kg body weight, every day for 14 consecutive days) significantly ameliorated all the tested parameters. Melatonin moderately increased SOD, CAT, GSH-Rd and GST activities, thereby counteracting the oxidative stress induced by ALA. Nevertheless, exogenous ALA caused a strong net rise in MDA and PC and a significant decrease in GSH when given together with ALA, melatonin antagonized these effects and largely protected the integrity of tissue structures. From the present data, the protection of melatonin against ALA oxidative stress is obviously, so it is well recommended to use melatonin in patients suffering from symptoms related to ALA accumulation.

Role of melatonin in modulation of oxidative stress induced by delta- aminolevulinic acid in adult male albino rats.