Learning deficits in C57BL/6J mice following perinatal arsenic exposure: Consequence of lower corticosterone receptor levels?

Martinez-Finley, Ebany J.; Ali, Abdul-Mehdi S.; Allan, Andrea M.

doi:10.1016/j.pbb.2009.09.006

Cited by 95 publications

(82 citation statements)

References 60 publications

(73 reference statements)

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“…45 Upon chronic exposure to arsenic, rats show significant memory impairment during the Morris water maze test 46-48 as well as decreased learning ability on novel object exploration. 49 On the other hand, mice exposed to chronic low-level arsenic exhibit gender-specific and dosedependent alterations on spontaneous locomotor activity, 50 while the mobility is reduced in rats. 51,52 The neurological impact on early developmental stage attract attention also because arsenic has been detected in baby rice cereal, which form the major arsenic exposure source.…”

Section: Figmentioning

confidence: 99%

The Effect of Chronic Arsenic Exposure in Zebrafish

et al. 2016

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Arsenic is a prevalent environmental toxin and a Group one human carcinogenic agent. Chronic arsenic exposure has been associated with many human diseases. The aim of this study is to evaluate zebrafish as an animal model to assess arsenic toxicity in elevated long-term arsenic exposure. With prolonged exposure (6 months) to various concentrations of arsenic from 50 ppb to 300 ppb, effects of arsenic accumulation in zebrafish tissues, and phenotypes were investigated. Results showed that there are no significant changes of arsenic retention in zebrafish tissues, and zebrafish did not exhibit any visible tumor formation under arsenic exposure conditions. However, the zebrafish demonstrate a dysfunction in their neurological system, which is reflected by a reduction of locomotive activity. Moreover, elevated levels of the superoxide dismutase (SOD2) protein were detected in the eye and liver, suggesting increased oxidative stress. In addition, the progenies of arsenic-treated parents displayed a smaller biomass (four-fold reduction in body weight) compared with those from their parental controls. This result indicates that arsenic may induce genetic or epigenetic changes that are then passed on to the next generation. Overall, this study demonstrates that zebrafish is a convenient vertebrate model with advantages in the evaluation of arsenic-associated neurological disorders as well as its influences on the offspring.

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Section: Figmentioning

confidence: 99%

The Effect of Chronic Arsenic Exposure in Zebrafish

et al. 2016

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“…For example, in utero and early life exposure of rodents even to 50 or 100 μg/μL of iAs through drinking water leads to learning and memory deficits in adult offspring [3,13]. In another study, perinatal mice exposure to low iAs concentration (55 μg/L) led to reduced performance in forced swim test and increased response time in learned helplessness [10].…”

Section: Introductionmentioning

confidence: 98%

Cortical Astrocytes Acutely Exposed to the Monomethylarsonous Acid (MMAIII) Show Increased Pro-inflammatory Cytokines Gene Expression that is Consistent with APP and BACE-1: Over-expression

et al. 2016

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Long-term exposure to inorganic arsenic (iAs) through drinking water has been associated with cognitive impairment in children and adults; however, the related pathogenic mechanisms have not been completely described. Increased or chronic inflammation in the brain is linked to impaired cognition and neurodegeneration; iAs induces strong inflammatory responses in several cells, but this effect has been poorly evaluated in central nervous system (CNS) cells.Because astrocytes are the most abundant cells in the CNS and play a critical role in brain homeostasis, including regulation of the inflammatory response, any functional impairment in them can be deleterious for the brain. We propose that iAs could induce cognitive impairment through inflammatory response activation in astrocytes. In the present work, rat cortical astrocytes were acutely exposed in vitro to the monomethylated metabolite of iAs (MMA III ), which accumulates in glial cells without compromising cell viability. MMA III LD 50 in astrocytes was 10.52 μM, however, exposure to sub-toxic MMA III concentrations (50 to 1000 nM) significantly increased IL-1β, IL-6, TNF-α, COX-2, and MIF-1 gene expression. These effects were consistent with amyloid precursor protein (APP) and β-secretase (BACE-1) increased gene expression, mainly for those MMA III concentrations that also induced TNF-α over-expression. Other effects of MMA III on cortical astrocytes included increased proliferative and metabolic activity. All tested MMA III concentrations led to an inhibition of intracellular lactate dehydrogenase (LDH) activity. Results suggest that MMA III induces important metabolic and functional changes in astrocytes that may affect brain homeostasis and that inflammation may play a major role in cognitive impairment-related pathogenicity in As-exposed populations.

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“…19,20) Rats and mice exposed to arsenic during gestation and early childhood exhibit behavioral deficits such as changes in locomotor activity, learning, memory, depression-like behavior and neuromotor reflex. [21][22][23] The development of the central nervous system (CNS) in neonatal rats is also affected by arsenic, and exposure to arsenic has been shown to cause neuronal death in the adult rat brain. 24) Sodium arsenite at a concentration of 5 µM induces cytotoxicity at a cellular level via acting as a sulfhydryl reagent, which binds to the free thiol groups of numerous enzymes, inhibiting their functions and depleting levels of glutathione (GSH), thus destroying cell metabolism.…”

Section: Sodium Arsenite Induces Neural Cell Death Via a Mitochondriamentioning

confidence: 99%

Role of Environmental Chemical Insult in Neuronal Cell Death and Cytoskeleton Damage

Aung

Tsukahara

Maekawa

et al. 2015

Biological & Pharmaceutical Bulletin

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Environmental influences, such as chemical exposure, have long been considered potential risk factors for neurodegenerative disorders, including neuromuscular diseases. However, no definitive links between environmental chemical exposure and a pathogenic mechanism of neurodegenerative disease has yet been established. In this study, we describe that exposure to arsenic, an environmental pollutant naturally found in drinking water, induces neuronal cell death and alteration of morphology, particularly neurite outgrowth and in the cytoskeleton of neurons. Since progressive cell loss accompanied by the alteration of neuronal structures and cytoskeleton is considered the major pathologic feature of neurodegenerative disorders, arsenic-induced neurotoxicity might contribute to an etiologic mechanism of some neurodegenerative diseases. Further, we discuss the importance of in vitro assay, particularly an embryonic toxicity test, for assessing the neurotoxicity of chemicals, because most of chemicals found in our environment remain to be evaluated regarding their neurotoxicity risk for neurodegenerative diseases.

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Learning deficits in C57BL/6J mice following perinatal arsenic exposure: Consequence of lower corticosterone receptor levels?

Cited by 95 publications

References 60 publications

The Effect of Chronic Arsenic Exposure in Zebrafish

The Effect of Chronic Arsenic Exposure in Zebrafish

Cortical Astrocytes Acutely Exposed to the Monomethylarsonous Acid (MMAIII) Show Increased Pro-inflammatory Cytokines Gene Expression that is Consistent with APP and BACE-1: Over-expression

Role of Environmental Chemical Insult in Neuronal Cell Death and Cytoskeleton Damage

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