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The protective properties of melatonin against aluminium‐induced neuronal injury
Author(s) -
AlOlayan Ebtesam M.,
ElKhadragy Manal F.,
Abdel Moneim Ahmed E.
Publication year - 2015
Publication title -
international journal of experimental pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.671
H-Index - 72
eISSN - 1365-2613
pISSN - 0959-9673
DOI - 10.1111/iep.12122
Subject(s) - melatonin , oxidative stress , neurotoxicity , glutathione , antioxidant , lipid peroxidation , apoptosis , nitric oxide , chemistry , neuroprotection , pharmacology , endocrinology , toxicity , medicine , biochemistry , enzyme , biology
Summary Aluminium (Al) toxicity is closely linked to the pathogenesis of Alzheimer's disease ( AD ). This experimental study investigated the neuroprotective effect of melatonin (Mel; 10 mg/kg bwt) on aluminium chloride (AlCl 3 ; 34 mg/kg bwt) induced neurotoxicity and oxidative stress in rats. Adult male albino Wistar rats were injected with AlCl 3 for 7 days. The effect on brain structure, lipid peroxidation ( LPO ), nitric oxide ( NO ) levels, glutathione ( GSH ) content, antioxidant enzymes ( SOD , CAT , GP x and GR ), apoptotic proteins (Bax and Bcl‐2) and an apoptotic enzyme (caspase‐3) was investigated. No apparent changes occurred following the injection of melatonin. Melatonin pretreatment of the AlCl 3 ‐administered rats reduced brain damage, and the tissues appeared like those of the control rats. Compared to treatment with AlCl 3 , pretreatment with melatonin decreased LPO and NO levels and increased the GSH content and antioxidant enzyme activity. Moreover, melatonin increased the levels of the anti‐apoptotic protein, Bcl‐2, decreased the levels of the pro‐apoptotic protein, Bax, and inhibited caspase‐3 activity. Therefore, our results indicate that melatonin may provide therapeutic value against aluminium‐induced oxidative stress and histopathological alternations in the rat brain and that these effects may be related to anti‐apoptotic and antioxidant activities.