Melatonin Ameliorates Cadmium-Induced Affective and Cognitive Impairments and Hippocampal Oxidative Stress in Rat

Lamtai, Mouloud; Azirar, Sofia; Zghari, Oussama; Ouakki, Sihame; Hessni, Aboubaker El; Mesfioui, Abdelhalem; Ouichou, Ali

doi:10.1007/s12011-020-02247-z

Cited by 37 publications

(13 citation statements)

References 60 publications

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“…In addition, exogenous administration of Mel could ameliorate the depressive-like behavior induced by Ni; this neurohormone significantly reduced immobility time in the FST. Consistent with other reports, it was found that Mel produces a variety of anxiolytic-like effects in different tests [ 24 , 37 , 38 ]. Also, Stefanovic et al showed that Mel elicited a real power antidepressant-like effect in the FST [ 39 ].…”

Section: Discussionsupporting

confidence: 90%

Neuroprotective effect of melatonin on nickel-induced affective and cognitive disorders and oxidative damage in rats

Lamtai

Ouakki

Zghari

et al. 2020

Environ Anal Health Toxicol

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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.

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Section: Discussionsupporting

confidence: 90%

Neuroprotective effect of melatonin on nickel-induced affective and cognitive disorders and oxidative damage in rats

Lamtai

Ouakki

Zghari

et al. 2020

Environ Anal Health Toxicol

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“…LPS treatment resulted in the death of hippocampal and cortical neurons, but did not lead to the death of cerebellar neurons, indicating that the local production of melatonin can protect cerebellar neurons from LPS toxicity ( 23 ). In addition to its pivotal role in improving neurobehavioral deficits, Mel is able to scavenge free radicals, stimulate antioxidant defenses of the cells, and decrease the activity of pro-oxidant enzymes ( 62 , 63 ).…”

Section: Discussionmentioning

confidence: 99%

Effects of Melatonin on Neurobehavior and Cognition in a Cerebral Palsy Model of plppr5−/− Mice

Sun

Jin

et al. 2021

Front. Endocrinol.

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Cerebral palsy (CP), a group of clinical syndromes caused by non-progressive brain damage in the developing fetus or infant, is one of the most common causes of lifelong physical disability in children in most countries. At present, many researchers believe that perinatal cerebral hypoxic ischemic injury or inflammatory injury are the main causes of cerebral palsy. Previous studies including our works confirmed that melatonin has a protective effect against convulsive brain damage during development and that it affects the expression of various molecules involved in processes such as metabolism, plasticity and signaling in the brain. Integral membrane protein plppr5 is a new member of the plasticity-related protein family, which is specifically expressed in brain and spinal cord, and induces filopodia formation as well as neurite growth. It is highly expressed in the brain, especially in areas of high plasticity, such as the hippocampus. The signals are slightly lower in the cortex, the cerebellum, and in striatum. Noteworthy, during development plppr5 mRNA is expressed in the spinal cord, i.e., in neuron rich regions such as in medial motor nuclei, suggesting that plppr5 plays an important role in the regulation of neurons. However, the existing literature only states that plppr5 is involved in the occurrence and stability of dendritic spines, and research on its possible involvement in neonatal ischemic hypoxic encephalopathy has not been previously reported. We used plppr5 knockout (plppr5−/−) mice and their wild-type littermates to establish a model of hypoxicischemic brain injury (HI) to further explore the effects of melatonin on brain injury and the role of plppr5 in this treatment in an HI model, which mainly focuses on cognition, exercise, learning, and memory. All the tests were performed at 3–4 weeks after HI. As for melatonin treatment, which was performed 5 min after HI injury and followed by every 24h. In these experiments, we found that there was a significant interaction between genotype and treatment in novel object recognition tests, surface righting reflex tests and forelimb suspension reflex tests, which represent learning and memory, motor function and coordination, and the forelimb grip of the mice, respectively. However, a significant main effect of genotype and treatment on performance in all behavioral tests were observed. Specifically, wild-type mice with HI injury performed better than plppr5−/− mice, regardless of treatment with melatonin or vehicle. Moreover, treatment with melatonin could improve behavior in the tests for wild-type mice with HI injury, but not for plppr5−/− mice. This study showed that plppr5 knockout aggravated HI damage and partially weakened the neuroprotection of melatonin in some aspects (such as novel object recognition test and partial nerve reflexes), which deserves further study.

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“…In the rat brain, sub‐chronic exposure to Cd for 30 days induced a significant reduction in antioxidant enzyme activity, including glutathione peroxidase, catalase, and superoxide dismutase, and an increase in malondialdehyde concentration in the hippocampus 71 . Another study also found that Cd significantly increased the levels of nitric oxide (NO) and lipid peroxidation in the rat hippocampus 72 . In addition, Cd can disrupt the homeostasis of intracellular free calcium and lead to the death of different neuronal cells in the brain.…”

Section: Discussionmentioning

confidence: 97%

Adolescent cadmium exposure impairs cognition and hippocampal neurogenesis in C57BL/6 mice

Wang

Abel

Storm

et al. 2021

Environmental Toxicology

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Cadmium (Cd) is a toxic heavy metal and a significant public health concern. Epidemiological studies suggest that Cd is a potential neurotoxicant, and its exposure is associated with cognitive deficits in children, adults, and seniors. Our previous study has found that adulthood‐only Cd exposure can impair cognition in mice. However, few studies have addressed the effects of Cd exposure during adolescence on cognitive behavior in animals later in life. In the present study, we exposed 4‐week‐old male C57BL/6 mice to 3 mg/L Cd via drinking water for 28 weeks and assessed their hippocampus‐dependent learning and memory. Cd did not affect anxiety or locomotor activity in the open field test. However, Cd exposure impaired short‐term spatial memory and contextual fear memory in mice. A separate cohort of 4‐week‐old mice was similarly exposed to Cd for 13 weeks to investigate the potential mechanism of Cd neurotoxicity on cognition. We observed that Cd‐treated mice had fewer adult‐born cells, adult‐born neurons, and a reduced proportion of adult‐born cells that differentiated into mature neurons in the subgranular zone of the dentate gyrus. These results suggest that Cd exposure from adolescence to adulthood is sufficient to cause cognitive deficits and impair key processes of hippocampal neurogenesis in mice.

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Melatonin Ameliorates Cadmium-Induced Affective and Cognitive Impairments and Hippocampal Oxidative Stress in Rat

Cited by 37 publications

References 60 publications

Neuroprotective effect of melatonin on nickel-induced affective and cognitive disorders and oxidative damage in rats

Neuroprotective effect of melatonin on nickel-induced affective and cognitive disorders and oxidative damage in rats

Effects of Melatonin on Neurobehavior and Cognition in a Cerebral Palsy Model of plppr5−/− Mice

Adolescent cadmium exposure impairs cognition and hippocampal neurogenesis in C57BL/6 mice

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