Arsenic speciation transported through the placenta from mother mice to their newborn pups

Jin, Yaping; Shi, Xi; Li, Xin; Lu, Chun-Wei; Li, Gexin; Xu, Yuanyuan; Qu, Chunqing; Niu, Yuhong; Sun, Guifan

doi:10.1016/j.envres.2005.11.006

Cited by 124 publications

(81 citation statements)

References 39 publications

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“…Arsenic species were measured by the method reported previously [40]. Briefly, 0.1 g of brain from pups was digested with 4 N NaOH solution at 100…”

Section: Arsenic Determination In Brain Tissuementioning

confidence: 99%

“…The enhancement of reactive oxygen species (ROS) and lipid peroxidation and the decreases in the activity of superoxide dismutase and glutathione-related enzymes induced by As could change the cellular redox status and lead to impairments of neurobehavioral function [35][36][37][38][39]. Arsenic is as a known neurotoxicant and is able to transverse the placental barrier and reaches to the conceptus in the case of maternal exposure and also crossed the blood-brain barrier (BBB) easily in our previous studies [40,41] and other researches [39,[42][43]. Itoh et al [24] reported that As may penetrate the BBB to modify CNS metabolism and function at low doses.…”

Section: Introductionmentioning

confidence: 99%

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Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

Shi

Guo

et al. 2010

J Biochem & Molecular Tox

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To better understand the effect of arsenic on central nervous system by prenatal and early life exposure, the oxidative stress and neurotransmitter metabolic enzymes were determined in offspring rats' brain cortex and hippocampus. Forty-eight pregnant rats were randomly divided into four groups, each group was given free access to drinking water that contained 0, 10, 50, and 100 mg/L NaAsO(2) from gestation day 6 (GD 6) until postnatal day 42 (PND 42). Once pups were weaned, they started to drink the same arsenic (As)-containing water as the dams. The level of malondialdehyde in 100 mg/L As-exposed pup's brain on PND 0 and cortex on PND 28 and 42 were significantly higher than in the control group (p < 0.05). Reduced glutathione (GSH) levels showed a clear decreasing trend in pup's cortex and hippocampus on PND 42. Activity of acetylcholinesterase was significantly higher in 100 mg/L As-exposed pup's hippocampus than in control group on PND 28 and 42. mRNA expression of glutamate decarboxylase (GAD(65) and GAD(67)) in 100 mg/L As-exposed pup's cortex or hippocampus on PND 28 and 42 were significantly higher than in control (p < 0.05). These alterations in the neurotransmitters and reduced antioxidant defence may lead to neurobehavioral and learning and memory changes in offspring rats.

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“…Arsenic species were measured by the method reported previously [40]. Briefly, 0.1 g of brain from pups was digested with 4 N NaOH solution at 100…”

Section: Arsenic Determination In Brain Tissuementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

Shi

Guo

et al. 2010

J Biochem & Molecular Tox

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“…Similarly, little information exists on early-life toxicity of methylarsonate and dimethylarsinate. Both inorganic arsenic and dimethylarsinate are transferred from the mother through the placenta and cross the immature bloodbrain barrier easily (Jin et al, 2006). Compared to that in the liver of newborn mice, dimethylarsinate as an organic metabolite is prevalent in the brain.…”

Section: Organic Arsenicmentioning

confidence: 99%

Scientific Opinion on Arsenic in Food

2009

EFSA Journal

856

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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“…iAs and its metabolites are eliminated through urine and feces, but an important proportion of them will accumulate in different tissues, including the brain [2]. iAs and its metabolites accumulate in the cerebral cortex, hippocampus, striatum, midbrain, thalamus, pons, medulla oblongata, and pituitary gland of rodents intoxicated with 2.5, 5, and 10 mg/kg/day of sodium arsenite [3,4].…”

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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Arsenic speciation transported through the placenta from mother mice to their newborn pups

Cited by 124 publications

References 39 publications

Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

Prenatal and early life arsenic exposure induced oxidative damage and altered activities and mRNA expressions of neurotransmitter metabolic enzymes in offspring rat brain

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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