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<p>Mercurial chloride (HgCl<sub>2</sub>) is a potent neurotoxin known to cause affective disorders and cognitive deficits through mechanisms involving oxidative stress, excitotoxicity, and neurotransmitter dysregulation. Melatonin (MEL) has demonstrated neuroprotective properties, including antioxidant and anti-inflammatory effects. This study aimed to assess the neuroprotective effects of MEL in mitigating HgCl<sub>2</sub>-induced anxiety, depression, cognitive deficits, and oxidative stress in adult male rats. Animals were divided into four groups: control, HgCl<sub>2</sub>-exposed, HgCl<sub>2</sub> + MEL-treated, and MEL-only groups. Behavioral assessments for anxiety, depression, and cognitive function were conducted using the open field test (OFT), elevated plus maze (EPM), forced swim test (FST), Y-maze, and Morris water maze (MWM). Oxidative stress markers, including lipid peroxidation (LPO), nitric oxide (NO) levels, and catalase (CAT) activity, were measured in the hippocampus. HgCl<sub>2</sub> exposure led to significant increases in anxiety-like and depression-like behaviors, as well as memory impairments. Importantly, co-administration of MEL effectively reversed these behaviors and significantly reduced hippocampal oxidative stress markers. MEL offers substantial neuroprotection against HgCl<sub>2</sub>-induced neurotoxicity, primarily through its antioxidant properties and ability to reduce oxidative stress.</p>

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Neuroprotective effects of melatonin on mercury-induced anxiety-like, depression-like, and memory deficits in rat

  • 期刊论文

  • 发表日期：

    2025年6月1日

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  • Sofia Azirar,
  • Mouloud Lamtai,
  • Abdelghafour El Hamzaoui,
  • Mohamed Yassine El Brouzi,
  • Laila Ibouzine-dine,
  • Aboubaker El Hessni,
  • Abdelhalem Mesfioui

摘要

Mercurial chloride (HgCl2) is a potent neurotoxin known to cause affective disorders and cognitive deficits through mechanisms involving oxidative stress, excitotoxicity, and neurotransmitter dysregulation. Melatonin (MEL) has demonstrated neuroprotective properties, including antioxidant and anti-inflammatory effects. This study aimed to assess the neuroprotective effects of MEL in mitigating HgCl2-induced anxiety, depression, cognitive deficits, and oxidative stress in adult male rats. Animals were divided into four groups: control, HgCl2-exposed, HgCl2 + MEL-treated, and MEL-only groups. Behavioral assessments for anxiety, depression, and cognitive function were conducted using the open field test (OFT), elevated plus maze (EPM), forced swim test (FST), Y-maze, and Morris water maze (MWM). Oxidative stress markers, including lipid peroxidation (LPO), nitric oxide (NO) levels, and catalase (CAT) activity, were measured in the hippocampus. HgCl2 exposure led to significant increases in anxiety-like and depression-like behaviors, as well as memory impairments. Importantly, co-administration of MEL effectively reversed these behaviors and significantly reduced hippocampal oxidative stress markers. MEL offers substantial neuroprotection against HgCl2-induced neurotoxicity, primarily through its antioxidant properties and ability to reduce oxidative stress.