Inhibitory Effects of Selenium on Arsenic-Induced Anxiety-/Depression-Like Behavior and Memory Impairment

Samad, Noreen; Rao, T. Srinivasa; Rehman, Muhammad Habib ur; Bhatti, Sheraz Ahmed; Imran, Imran

doi:10.1007/s12011-021-02679-1

Cited by 27 publications

(21 citation statements)

References 58 publications

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“…These dissected brains were weighed and n homogenized separately in 1:10 w/v of 0.1 M phosphate buffer of pH 7.4 and centrifuged at 4000 rpm for 5 min at reduced temperature. After centrifugation, the pellet was discarded and brain tissue supernatant was isolated and used for the evaluation of biochemical parameters to associate the antioxidant potential of test treatments with protection from kindling progression and associated behavioral impairment ( Samad et al, 2021 ).…”

Section: Methodsmentioning

confidence: 99%

“…In another study by Tawfik et al, the sildenafil in combination with selenium modulated the angiogenesis and combated the oxidative stress in PTZ-kindled mice ( Tawfik et al, 2018 ). To assess the neuroprotective potential, Samad et al reported the improved behavioral and biochemical outcomes by selenium supplementation in arsenic intoxicated rats ( Samad et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

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Combination of levetiracetam with sodium selenite prevents pentylenetetrazole-induced kindling and behavioral comorbidities in rats

Rehman

Farooq

Javaid

et al. 2022

Saudi Pharmaceutical Journal

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Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Combination of levetiracetam with sodium selenite prevents pentylenetetrazole-induced kindling and behavioral comorbidities in rats

Rehman

Farooq

Javaid

et al. 2022

Saudi Pharmaceutical Journal

Self Cite

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“…Major depressive disorder is a highly disabling psychiatric syndrome associated with deficits of specific subpopulations of cortical GABA-ergic interneurons[ 1 , 2 ]. We were pleased to read the article by Samad et al [ 3 ]. Their work highlights that Se, as a dietary source and/or supplement, is an effective therapy for As poisoning and its associated disorders.…”

Section: To the Editormentioning

confidence: 99%

Sodium selenite may be not the optimal speciation as an effective therapy for arsenic-induced anxiety-/depression-like behavior

Ren¹,

Wang²,

He³

2022

WJP

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Major depressive disorder is a serious and prevalent neuropsychiatric disorder, affecting more than 350 million people worldwide. Here, sodium selenite (SS) was selected as the selenite supplement to improve the behavior in a mouse model of depression induced by As. SS may be not the optimal speciation for selenite supplementation and the source of the SS used in the study was not disclosed. There are many mouse models of depression and anxiety; however, in the current study, a classical mouse model of depression was not used. Thus, several questions still need to be further discussed. Taken together, the results indicate that SS may be not the optimal speciation as an effective therapy for As-induced anxiety-/depression-like behavior.

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“…Selenium co-administration can protect against arsenic-induced behavioral deficits in rats through a mechanism involving anti-inflammation, antioxidation, and anti-apoptosis ( Figure 6 ) [ 77 ]. In another study by Samad and colleagues, selenium supplementation through drinking water ameliorated arsenic-induced anxiety/depression and memory deficits in rats [ 78 ]. In chickens exposed to arsenic at a subacute dose, selenium (up to 10 mg/kg) prevented oxidative damage, neurotransmitter disorders, and apoptosis in the brain [ 79 ].…”

Section: Management and Control Of Arsenic-induced Neurological Deficitsmentioning

confidence: 99%

Exposure to Environmental Arsenic and Emerging Risk of Alzheimer’s Disease: Perspective Mechanisms, Management Strategy, and Future Directions

Rahman

Hannan

Uddin

et al. 2021

Toxics

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Alzheimer’s disease (AD) is one of the most prevailing neurodegenerative diseases, characterized by memory dysfunction and the presence of hyperphosphorylated tau and amyloid β (Aβ) aggregates in multiple brain regions, including the hippocampus and cortex. The exact etiology of AD has not yet been confirmed. However, epidemiological reports suggest that populations who were exposed to environmental hazards are more likely to develop AD than those who were not. Arsenic (As) is a naturally occurring environmental risk factor abundant in the Earth’s crust, and human exposure to As predominantly occurs through drinking water. Convincing evidence suggests that As causes neurotoxicity and impairs memory and cognition, although the hypothesis and molecular mechanism of As-associated pathobiology in AD are not yet clear. However, exposure to As and its metabolites leads to various pathogenic events such as oxidative stress, inflammation, mitochondrial dysfunctions, ER stress, apoptosis, impaired protein homeostasis, and abnormal calcium signaling. Evidence has indicated that As exposure induces alterations that coincide with most of the biochemical, pathological, and clinical developments of AD. Here, we overview existing literature to gain insights into the plausible mechanisms that underlie As-induced neurotoxicity and the subsequent neurological deficits in AD. Prospective strategies for the prevention and management of arsenic exposure and neurotoxicity have also been discussed.

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Inhibitory Effects of Selenium on Arsenic-Induced Anxiety-/Depression-Like Behavior and Memory Impairment

Cited by 27 publications

References 58 publications

Combination of levetiracetam with sodium selenite prevents pentylenetetrazole-induced kindling and behavioral comorbidities in rats

Combination of levetiracetam with sodium selenite prevents pentylenetetrazole-induced kindling and behavioral comorbidities in rats

Sodium selenite may be not the optimal speciation as an effective therapy for arsenic-induced anxiety-/depression-like behavior

Exposure to Environmental Arsenic and Emerging Risk of Alzheimer’s Disease: Perspective Mechanisms, Management Strategy, and Future Directions

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