Exploring the neuroprotective role of melatonin against nickel-induced neurotoxicity in the left hippocampus

• Published in: Biometals 2024-12, Vol.37 (6), p.1457-1469
• Main Authors: El Brouzi, Mohamed Yassine, Lamtai, Mouloud, Fath, Nada, Rezqaoui, Ayoub, Zghari, Oussama, El Hamzaoui, Abdelghafour, Ibouzine-dine, Laila, El Hessni, Aboubaker, Mesfioui, Abdelhalem
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants; Antioxidants - metabolism; Antioxidants - pharmacology; Biochemistry; Biomedical and Life Sciences; Catalase; Cell Biology; Cognitive ability; Damage prevention; Enzymatic activity; Exposure; Heavy metals; Hippocampus; Hippocampus - drug effects; Hippocampus - metabolism; Injection; L-Lactate dehydrogenase; Lactate dehydrogenase; Life Sciences; Male; Medicine/Public Health; Melatonin; Melatonin - administration & dosage; Melatonin - pharmacology; Microbiology; Neurological diseases; Neuroprotection; Neuroprotective Agents - pharmacology; Neurotoxicity; Nickel; Nickel - toxicity; Oxidative stress; Oxidative Stress - drug effects; Pharmacology/Toxicology; Plant Physiology; Rats; Rats, Wistar; Reactive oxygen species; Reactive Oxygen Species - metabolism; Side effects; Superoxide dismutase
• ISSN: 0966-0844; 1572-8773; 1572-8773
• DOI: 10.1007/s10534-024-00618-w

Previous studies have demonstrated that the hippocampus, a crucial region for memory and cognitive functions, is particularly vulnerable to adverse effects of exposure to heavy metals. Nickel (Ni) is a neurotoxic agent that, primarily induces oxidative stress, a process known to contribute to cellular damage, which consequently affects neurological functions. The antioxidant properties of melatonin are a promising option for preventing the adverse effects of Ni, especially by protecting cells against oxidative stress and related damage. In our investigation of the potential neuroprotective effects of melatonin against Ni-induced neurotoxicity, we chose to administer melatonin through intraperitoneal injection in rats following an intrahippocampal injection of Ni into the left hippocampus. This approach allows us a targeted investigation into the influence of melatonin on the neurotoxic effects of Ni, particularly within the crucial context of the hippocampus. In the present study, we demonstrated that melatonin efficiency reduced lactate dehydrogenase level, and preserved antioxidant enzyme activities in Ni-exposed hippocampal tissue. It also mitigated the decline in superoxide dismutase and catalase activities. On the other hand, melatonin could act directly by reducing reactive oxygen species Ni-induced overproduction. Taking to gather these two potential mechanisms of action could be responsible for the adverse effect of Ni on the behavioral alteration observed in our study. This study provides significant insights into the potential of melatonin to mitigate the detrimental effects of Ni on the brain, particularly into the hippocampal region, suggesting its possible implications for the treatment of neurological disorders related to Ni exposure.