Affective Behavior Dysregulation Was Induced by Chronic Administration of Copper in Wistar Rats

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

doi:10.4236/nm.2019.102009

Cited by 8 publications

(4 citation statements)

References 60 publications

(57 reference statements)

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“…A significant association between Cu and neurobehavioral performance was revealed [17][18][19]. Our previous data have demonstrated that chronic Cu exposure modulates affective behaviors [20].…”

Section: Introductionmentioning

confidence: 83%

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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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Section: Introductionmentioning

confidence: 83%

“…Group IV: animals were administered Copper (1 mg/kg) once daily. The concentrations of Cu used in this study were chosen based on our previous experiment evaluating neurobehavioral alterations in rat [20].…”

Section: Animals and Experimental Conditionsmentioning

confidence: 99%

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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“…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: 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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“…A luminum (Al) neurotoxicity is a major factor influencing affective and cognitive disorders (Zghari et al, 2018). A growing body of literature suggests that heavy metals, including cadmium, copper and nickel, produce affective and cognitive disorders in rat brain (Lamtai et al, 2018(Lamtai et al, , 2019(Lamtai et al, , 2020a(Lamtai et al, , b, 2021El-Brouzi et al, 2020). Neurodegenerative diseases such as Alzheimer's disease (AD) have also been linked to Al exposure (Esparza et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Neuroprotective Effects of Melatonin Against Neurotoxicity Induced by Intrahippocampal Injection of Aluminum in Male Wistar Rats: Possible Involvement of Oxidative Stress Pathway

Zghari¹,

Lamtai²,

Azirar³

et al. 2023

AAVS

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| Aluminum (Al) is a well-established neurotoxicant, affecting various regions of the brain and causing many neuropathological and neurobehavioral abnormalities as well as oxidative stress (OS). Conversely, melatonin (MEL) has been considered as an antidepressant, anxiolytic substance and protects neurons from OS. The present study was designed to evaluate the neuroprotection effect of MEL against Al neurotoxicity and OS in male Wistar rats. Rats received an intraperitoneal and/or a single intrahippocampal injection of NaCl, MEL or AlCl 3 . Before two weeks of intrahippocampal surgery period, MEL (4 mg/kg) was intraperitoneally injected (Group II and Group IV). Thereafter, control group (group I) received 2 µl NaCl (0.9%) and groups III and IV received 2 µl AlCl 3 (2 mg/kg) intracerebrally into the right ventral hippocampus. Five days after treatment period, all the rats were subjected to the neurobehavioral tests. The animals were then decapitated and the hippocampus was removed. Biochemical parameters of OS and the histology of Cornu Ammonis 3 (CA3) area of the hippocampus were evaluated. The results clearly showed that Al induced anxiety and depressive-like behaviour and cognitive impairment. In the hippocampus, Al also increased the levels of lipid peroxidation (LPO) and nitric oxide (NO) and reduced the activity of superoxide dismutase (SOD) as well mediates brain damage in CA3 hippocampal area. These alterations were reversed by MEL. It can be concluded that, by exerting its properties against the oxidative action of this metal in the hippocampus, MEL may play a potential role in protecting against the behavioral and histopathological alterations induced by Al.

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Affective Behavior Dysregulation Was Induced by Chronic Administration of Copper in Wistar Rats

Cited by 8 publications

References 60 publications

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

Neuroprotective Effects of Melatonin Against Neurotoxicity Induced by Intrahippocampal Injection of Aluminum in Male Wistar Rats: Possible Involvement of Oxidative Stress Pathway

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