The present work is carried out to explore the neuroprotective potential of Melatonin(Mel), on Ni-induced neurobehavioral, biochemical and histological alterations in male and female rats. The rats were intraperitoneally administered by nickel chloride (NiCl2, 1 mg/kg) and Mel (4 mg/kg) for 60 days. A neurobehavioral assessment was performed. Biochemical determinations of oxidative stress (OS) levels, and histological analysis of hippocampal tissues were also performed. Results showed that Nickel (Ni) treatment increased anxiety-like and depression-like behavior in rats. Besides, cognitive behavior on the Morris water maze was compromised following Ni treatment. Alongside this, Ni elevated hippocampal OS markers like lipid peroxidation and nitric oxide formation with a decrease in superoxide dismutase and catalase activities. Histological observations confirmed these results. Significantly, Mel administration alleviated neurobehavioral changes in Ni-treated rats of both genders. Also, Mel attenuated Ni-induced OS and increased the activities of antioxidant enzymes. The histopathological studies in the hippocampus supported that Mel markedly reduced the Ni-induced neuronal loss. In conclusion, this study suggests that Mel has a neuroprotective effect against Ni-induced neurobehavioral alterations, which may be related to lowering OS in the hippocampus.
Aluminum (Al) is one of the more widespread metals in the environment used in various fields and the most abundant known for its neurotoxicity in both humans and animals and could be a potential factor inducing behavioral changes, oxidative stress (OS) and loss of synapses and neurons in the hippocampal and cerebral cortical areas. The main objective of this study is to determine the short-term impact of a single 2 μl intracerebral injection of AlCl3 at different doses on the right hippocampus on affective and cognitive behaviour, on levels of oxidative stress and morphological changes in male Wistar rats. Rats were treated with a single intrahippocampal injection of 2 μL of NaCl (0.9%) (Control) or successively with 2 μL of AlCl3 at 0.5 mg/Kg (Al-0.5), 1 mg/Kg (Al-1) and 2 mg/Kg (Al-2). Five days following surgical procedures, neurobehavioral tests were performed for all groups (OFT, EPM, FST, Y-maze and MWM) and the brain were taken to isolate the hippocampus from adjacent tissues to prepare homogenates for the determination of oxidative stress markers and to examine the morphological change in CA3 hippocampal area. The results clearly demonstrate that Al induced anxiety and depressive-like behaviours, cognitive deficit, increased lipid peroxidation (LPO), nitric oxide (NO) levels, decreased superoxide dismutase (SOD) activity in the hippocampus and mediates progressive alterations characterized by disorganization in the pyramidal cellular arrangement and a decrease in neuronal density in the CA3 hippocampal area. In conclusion, a single intrahippocampal injection of Al induced anxiety-like, depression-like, memory impairment, OS and morphological alterations in the hippocampus.
| Aluminum (Al) is a well-established neurotoxicant, affecting various regions of the brain and causing many neuropathological and neurobehavioral abnormalities as well as oxidative stress (OS). Conversely, melatonin (MEL) has been considered as an antidepressant, anxiolytic substance and protects neurons from OS. The present study was designed to evaluate the neuroprotection effect of MEL against Al neurotoxicity and OS in male Wistar rats. Rats received an intraperitoneal and/or a single intrahippocampal injection of NaCl, MEL or AlCl 3 . Before two weeks of intrahippocampal surgery period, MEL (4 mg/kg) was intraperitoneally injected (Group II and Group IV). Thereafter, control group (group I) received 2 µl NaCl (0.9%) and groups III and IV received 2 µl AlCl 3 (2 mg/kg) intracerebrally into the right ventral hippocampus. Five days after treatment period, all the rats were subjected to the neurobehavioral tests. The animals were then decapitated and the hippocampus was removed. Biochemical parameters of OS and the histology of Cornu Ammonis 3 (CA3) area of the hippocampus were evaluated. The results clearly showed that Al induced anxiety and depressive-like behaviour and cognitive impairment. In the hippocampus, Al also increased the levels of lipid peroxidation (LPO) and nitric oxide (NO) and reduced the activity of superoxide dismutase (SOD) as well mediates brain damage in CA3 hippocampal area. These alterations were reversed by MEL. It can be concluded that, by exerting its properties against the oxidative action of this metal in the hippocampus, MEL may play a potential role in protecting against the behavioral and histopathological alterations induced by Al.
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