Moderate perinatal arsenic exposure alters neuroendocrine markers associated with depression and increases depressive-like behaviors in adult mouse offspring

Martinez, Ebany J.; Kolb, Brian; Bell, A. L. Loomis; Savage, Daniel D.; Allan, Andrea M.

doi:10.1016/j.neuro.2008.05.004

Cited by 81 publications

(93 citation statements)

References 52 publications

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“…Depressive syndromes have been reported in Gulf War veterans (McDiarmid et al, 2002). Other heavy metals induce also depressive-like behaviors in mouse offspring (Onishchenko et al, 2007;Martinez et al, 2008). It has been suggested that impairment in hippocampal function may be involved in the etiology of depression (Warner-Schmidt and Duman, 2006).…”

Section: Discussionmentioning

confidence: 99%

Uranium modifies or not behavior and antioxidant status in the hippocampus of rats exposed since birth

et al. 2015

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-In view of the known sensitivity of the developing central nervous system to pollutants, we sought to assess the effects of exposure to uranium (U) -a heavy metal naturally present in the environment -on the behavior of young rats and the impact of oxidative stress on their hippocampus. Pups drank U (in the form of uranyl nitrate) at doses of 10 or 40 mg.L -1 for 10 weeks from birth. Control rats drank mineral water. Locomotor activity in an open field and practice effects on a rotarod device decreased in rats exposed to 10 mg.L -1 (respectively, -19.4% and -51.4%) or 40 mg.L -1 (respectively, -19.3% and -55.9%) in compared with control rats. Anxiety (+37%) and depressive-like behavior (-50.8%) were altered by U exposure only at 40 mg.L -1 . Lipid peroxidation (+35%) and protein carbonyl concentration (+137%) increased significantly after exposure to U at 40 mg.L -1 . A significant increase in superoxide dismutase (SOD, +122.5%) and glutathione peroxidase (GPx, +13.6%) activities was also observed in the hippocampus of rats exposed to 40 mg.L -1 . These results demonstrate that exposure to U since birth alters some behaviors and modifies antioxidant status.

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Section: Discussionmentioning

confidence: 99%

Uranium modifies or not behavior and antioxidant status in the hippocampus of rats exposed since birth

et al. 2015

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“…Exposure of mouse dams to relatively low levels of arsenic (50 µg arsenate/L) during pregnancy and lactation resulted in changes in the neuroendocrine markers associated with depression and depressivelike behaviours in affected adult C57BL/6J mouse offspring (Martinez et al, 2008). The results suggested that perinatal arsenic exposure may disrupt the regulatory interactions between the hypothalamic-pituitary-adrenal axis and the serotonergic system in the dorsal hippocampal formation in a manner that predisposes affected offspring towards depressive-like behaviour.…”

Section: Inorganic Arsenicmentioning

confidence: 98%

Scientific Opinion on Arsenic in Food

2009

EFSA Journal

857

220

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The EFSA Panel on Contaminants in the Food Chain (CONTAM Panel) assessed the risks to human health related to the presence of arsenic in food. More than 100,000 occurrence data on arsenic in food were considered with approximately 98 % reported as total arsenic. Making a number of assumptions for the contribution of inorganic arsenic to total arsenic, the inorganic arsenic exposure from food and water across 19 European countries, using lower bound and upper bound concentrations, has been estimated to range from 0.13 to 0.56 µg/kg bodyweight (b.w.) per day for average consumers, and from 0.37 to 1.22 µg/kg b.w. per day for 95 th percentile consumers. Dietary exposure to inorganic arsenic for children under three years of age is in general estimated to be from 2 to 3-fold that of adults. The CONTAM Panel concluded that the provisional tolerable weekly intake (PTWI) of 15 µg/kg b.w. established by the Joint FAO/WHO Expert Committee on Food Additives (JECFA) is no longer appropriate as data had shown that inorganic arsenic causes cancer of the lung and urinary bladder in addition to skin, and that a range of adverse effects had been reported at exposures lower than those reviewed by the JECFA. The CONTAM Panel modelled the dose-response data from key for providing consumption information and calculating exposure, the partners of the EFSA project on the "Individual food consumption data and exposure" coordinated by Ghent University (Department of Public Health, University Hospital, Ghent University, Belgium), and RIKILT (Institute of Food Safety, Wageningen, The Netherlands) for the accessibility of the exposure assessment tools. 4 Table of contents shows now the fourth level of subheadings. 5 An error in the interpretation of the total number of the population in the study of Rahman et al. (2006a) was discovered (Table 41). The BMDL was recalculated and as a consequence it was not considered a potential reference point. The text in the opinion, Table 43 and Appendix were revised accordingly. In addition, the header of the "total number of cases" was replaced by "total number of individuals" in Tables 40-42 and the erroneous units were corrected to µg/L in the text below SUMMARYArsenic is a metalloid that occurs in different inorganic and organic forms, which are found in the environment both from natural occurrence and from anthropogenic activity. The inorganic forms of arsenic are more toxic as compared to the organic arsenic but so far most of the occurrence data in food collected in the framework of official food control are still reported as total arsenic without differentiating the various arsenic species. The need for speciation data is evident because several investigations have shown that especially in seafood most of the arsenic is present in organic forms that are less toxic. Consequently, a risk assessment not taking into account the different species but considering total arsenic as being present exclusively as inorganic arsenic would lead to a considerable overestimation of the health risk rel...

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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]. However the mechanisms underlying such neurotoxic effects that lead to As-associated cognitive dysfunction have not been completely elucidated.…”

Section: Introductionmentioning

confidence: 98%

“…However, stronger evidence from exposed populations and experimental studies have linked iAs exposure with cognitive impairment [5][6][7][8]. In exposed populations, a decreased verbal IQ in a dose-response manner has been reported in children with high urinary As concentration [9], and cognitive impairment was also found in a study conducted with children exposed to low iAs levels [10,11]. In adult populations, a significant correlation between exposure to As and an impaired cognitive ability even at As concentrations below the EPA standards (10 μg/L) for drinking water has been reported also [12].…”

Section: Introductionmentioning

confidence: 99%

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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Moderate perinatal arsenic exposure alters neuroendocrine markers associated with depression and increases depressive-like behaviors in adult mouse offspring

Cited by 81 publications

References 52 publications

Uranium modifies or not behavior and antioxidant status in the hippocampus of rats exposed since birth

Uranium modifies or not behavior and antioxidant status in the hippocampus of rats exposed since birth

Scientific Opinion on Arsenic in Food

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

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