El Brouzi Mohamed Yassine, Lamtai Mouloud, Fath Nada, Rezqaoui Ayoub, Zghari Oussama, El Hamzaoui Abdelghafour, Ibouzine-Dine Laila, El Hessni Aboubaker, Mesfioui Abdelhalem
Laboratory of Biology and Health, Neurosciences, Neuro-Immunology and Behaviour Unit, Faculty of Science, Ibn Tofail University, Kenitra, Morocco.
Compared Anatomy Unit, School of Veterinary Medicine, Hassan II Institute of Agronomy and Veterinary Medicine, Rabat, Morocco.
Biometals. 2024 Dec;37(6):1457-1469. doi: 10.1007/s10534-024-00618-w. Epub 2024 Jul 26.
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.
先前的研究表明，海马体作为记忆和认知功能的关键区域，特别容易受到重金属暴露的不利影响。镍（Ni）是一种神经毒性剂，主要诱导氧化应激，这一过程已知会导致细胞损伤，进而影响神经功能。褪黑素的抗氧化特性是预防镍的不利影响的一个有前景的选择，特别是通过保护细胞免受氧化应激和相关损伤。在我们对褪黑素对镍诱导的神经毒性的潜在神经保护作用的研究中，我们选择在向大鼠左侧海马体内注射镍后，通过腹腔注射给予褪黑素。这种方法使我们能够有针对性地研究褪黑素对镍神经毒性作用的影响，特别是在海马体这一关键背景下。在本研究中，我们证明褪黑素能降低镍暴露海马组织中的乳酸脱氢酶水平，并保留抗氧化酶活性。它还减轻了超氧化物歧化酶和过氧化氢酶活性的下降。另一方面，褪黑素可以通过减少镍诱导的活性氧过量产生而直接发挥作用。综合来看，这两种潜在的作用机制可能是镍对我们研究中观察到的行为改变产生不利影响的原因。这项研究为褪黑素减轻镍对大脑，特别是海马体区域的有害影响的潜力提供了重要见解，表明其对治疗与镍暴露相关的神经疾病可能具有的意义。
