Effect of Chronic Administration of Cadmium on Anxiety-Like, Depression-Like and Memory Deficits in Male and Female Rats: Possible Involvement of Oxidative Stress Mechanism

Lamtai, Mouloud; Chaibat, Jihane; Ouakki, Sihame; Berkiks, Inssaf; Rifi, El Housseine; Hessni, Aboubaker El; Mesfioui, Abdelhalem; Hbibi, Ali Tadlaoui; Ahyayauch, Hassna; Essamri, Azzouz; Ouichou, Ali

doi:10.4236/jbbs.2018.85016

Cited by 31 publications

(10 citation statements)

References 89 publications

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“…The forced swim test is a widely used test to evaluate depressive disorders 24 . The increase in the duration of immobility that is seen in the cadmium alone group is indicative of anxiety as earlier documented 25 , 37 . Remarkably, gallic acid and ascorbic acid treated groups reduced significantly the duration of immobility indicating their anti-depressive like potential in cadmium-induced toxicity.…”

Section: Discussionsupporting

confidence: 73%

Gallic and ascorbic acids supplementation alleviate cognitive deficits and neuropathological damage exerted by cadmium chloride in Wistar rats

Adebiyi

Adigun

David-Odewumi

et al. 2022

Sci Rep

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Cadmium is a highly neurotoxic heavy metal that interferes with DNA repair mechanisms via generation of reactive oxygen species. The potentials of polyphenols and antioxidants as effective protective agents following heavy metal-induced neurotoxicity are emerging. We therefore explored the neuroprotective potentials of gallic and ascorbic acids in CdCl2-induced neurotoxicity. Seventy-two Wistar rats were divided into six groups. Group A received distilled water, B: 3 mg/kg CdCl2, C: 3 mg/kg CdCl2 + 20 mg/kg gallic acid (GA), D: 3 mg/kg CdCl2 + 10 mg/kg ascorbic acid (AA), E: 20 mg/kg GA and F: 10 mg/kg AA orally for 21 days. Depression, anxiety, locomotion, learning and memory were assessed using a battery of tests. Neuronal structure and myelin expression were assessed with histological staining and immunofluorescence. The Morris Water Maze test revealed significant increase in escape latency in CdCl2 group relative to rats concurrently treated with GA or AA. Similarly, time spent in the target quadrant was reduced significantly in CdCl2 group relative to other groups. Concomitant administration of gallic acid led to significant reduction in the durations of immobility and freezing that were elevated in CdCl2 group during forced swim and open field tests respectively. Furthermore, GA and AA restored myelin integrity and neuronal loss observed in the CdCl2 group. We conclude that gallic and ascorbic acids enhance learning and memory, decrease anxiety and depressive-like behavior in CdCl2-induced neurotoxicity with accompanying myelin-protective ability.

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Section: Discussionsupporting

confidence: 73%

Gallic and ascorbic acids supplementation alleviate cognitive deficits and neuropathological damage exerted by cadmium chloride in Wistar rats

Adebiyi

Adigun

David-Odewumi

et al. 2022

Sci Rep

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“…The estrogens were found to favorite the Cu retention [74], which makes the females more vulnerable to the neurotoxic effects of Cu. The sex-related effect is shown also for other metals such Cd, Ni and Al [75][76][77]. Further experiences are needed to explicate the gender difference in the neurocognitive effect of this metal.…”

Section: Discussionmentioning

confidence: 93%

Chronic copper exposure leads to hippocampus oxidative stress and impaired learning and memory in male and female rats

et al. 2020

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Environmental and occupational exposures to copper (Cu) play a pivotal role in the etiology of some neurological diseases and reduced cognitive functions. However, the precise mechanisms of its effects on cognitive function have not been yet thoroughly established. In our study, we aimed to investigate the behavior and neurochemical alterations in hippocampus of male and female rats, chronically exposed to copper chloride (CuCl 2 ) and the possible involvement of oxidative stress. Twenty-four rats, for each gender, were divided into control and three test groups (n = 6), and were injected intraperitoneally with saline (0.9% NaCl) or CuCl 2 (0.25 mg/kg, 0.5 mg/kg and 1 mg/kg) for 8 weeks. After the treatment period, Y-maze test was used for the evaluation of spatial working memory and the Morris Water Maze (MWM) to test the spatial learning and memory. Biochemical determination of oxidative stress levels in hippocampus was performed. The main results of the present work are working memory impairment in spatial Y-maze which induced by higher Cu intake (1 mg/kg) in male and female rats. Also, In the MWM test, the spatial learning and memory were significantly impaired in rats treated with Cu at dose of 1 mg/kg. Additionally, markers of oxidative stress such as catalase, superoxide dismutase, lipid peroxidation products and nitric oxide levels were significantly altered following Cu treatments. These data propose that compromised behavior following Cu exposure is associated with increase in oxidative stress.

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“…Our previous study showed that chronic Ni exposure induced depression-like, anxiety-like, memory deficit, and alterations in OS markers in the hippocampus [13], a crucial brain region in learning, memory processes, and emotion regulation [14,15]. These effects are similar to those induced by other heavy metals such as Copper(Cu), Cadmium(Cd) and Aluminum(Al) [16][17][18][19]. Certain…”

Section: Introductionmentioning

confidence: 89%

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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Effect of Chronic Administration of Cadmium on Anxiety-Like, Depression-Like and Memory Deficits in Male and Female Rats: Possible Involvement of Oxidative Stress Mechanism

Cited by 31 publications

References 89 publications

Gallic and ascorbic acids supplementation alleviate cognitive deficits and neuropathological damage exerted by cadmium chloride in Wistar rats

Gallic and ascorbic acids supplementation alleviate cognitive deficits and neuropathological damage exerted by cadmium chloride in Wistar rats

Chronic copper exposure leads to hippocampus oxidative stress and impaired learning and memory in male and female rats

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

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