Preliminary morphological and morphometric study of rat cerebellum following sodium arsenite exposure during rapid brain growth (RBG) period

Dhar, Pushpa; Mohari, Nivedita; Mehra, Reeti

doi:10.1016/j.tox.2007.01.024

Cited by 40 publications

(28 citation statements)

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“…Various studies have proven that As exposure led children to brain-related disorders such as delaying of intelligent development and decline of cognitive function during rapid brain-developing times in human. As caused unusual migration of neurons and postponed neuronal maturation during brain-developmental period of rats (Dhar et al 2007). Abnormal changes of morphology of neuronal structure and axons were also found in another 1 3 study (R´ros et al 2009).…”

Section: Introductionmentioning

confidence: 70%

Taurine resumed neuronal differentiation in arsenite-treated N2a cells through reducing oxidative stress, endoplasmic reticulum stress, and mitochondrial dysfunction

et al. 2014

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The goal of the study is to investigate the preventive effect of taurine against arsenite-induced arrest of neuronal differentiation in N2a cells. Our results revealed that taurine reinstated the neurite outgrowth in arsenite-treated N2a cells. Meanwhile, arsenite-induced oxidative stress and mitochondrial dysfunction as well as degradation of mitochondria DNA (mtDNA) were also inhibited by co-treatment of taurine. Since oxidative stress and mitochondrial dysfunction is closely associated with endoplasmic reticulum (ER) stress, we further examined indicators of ER stress, 78 kDa glucose-regulated protein (GRP78), and C/EBP-homologous protein (CHOP) protein expression. The results demonstrated that taurine significantly reduced arsenite-induced ER stress in N2a cells. In the parallel experiment, arsenite-induced disruption of intracellular calcium homeostasis was also ameliorated by taurine. The proven bio-function of taurine preserved a preventive effect against deleteriously cross-talking between oxidative stress, mitochondria, and ER. Overall, the results of the study suggested that taurine reinstated neuronal differentiation by inhibiting oxidative stress, ER stress, and mitochondrial dysfunction in arsenite-treated N2a cells.

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Section: Introductionmentioning

confidence: 70%

Taurine resumed neuronal differentiation in arsenite-treated N2a cells through reducing oxidative stress, endoplasmic reticulum stress, and mitochondrial dysfunction

et al. 2014

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“…Neural tube effects are a consistent finding in experimental studies (Hill et al, 2008), but there are few studies investigating such effects in human populations and no convincing data (Shalat et al, 1996;Brender et al, 2006). Also, findings of aberrant migration and delayed maturation of Purkinje cells following low-dose prenatal arsenic exposure in rats (Dhar et al, 2007) warrant further studies on early human development. Nevertheless, studies on pregnant mice given periodate-oxidized adenosine, known to inhibit arsenic methylation , showed increased developmental toxicity from arsenic (Lammon et al, 2003).…”

Section: Inorganic Arsenicmentioning

confidence: 98%

Scientific Opinion on Arsenic in Food

2009

EFSA Journal

880

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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“…Previous research reported dysfunctions in cerebral nitric oxide (NO) production (Zarazua et al, 2006). Arsenic exposure also affects brain development, particularly cerebellar Purkinje cells (Dhar et al, 2007), adversely affecting cognitive development (Rodriguez et al , 2002.…”

Section: Accepted M Manuscriptmentioning

confidence: 99%

Locomotor activity and sensory – motor developmental alterations in rat offspring exposed to arsenic prenatally and via lactation

Gumilar

Lencinas

Bras

et al. 2015

Neurotoxicology and Teratology

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Please cite this article as: Fernanda Gumilar, Ileana Lencinas, Cristina Bras, Leda Giannuzzi, Alejandra Minetti, Locomotor activity and sensory-motor developmental alterations in rat offspring exposed to Arsenic prenatally and via lactation, Neurotoxicology and Teratology (2015), doi: 10.1016/j.ntt.2015 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.A C C E P T E D M A N U S C R I P T an open field were assessed in 90-day-old offspring. Results show that rats exposed to low iAs concentrations through drinking water during early development evidence a delay in the development of sensory-motor reflexes. A C C E P T E D M A N U S C R I P T ACCEPTED MANUSCRIPTBoth FOB procedure and open-field tests showed a decrease in locomotor activity in adult rats. This study reveals that exposure to the above-mentioned iAs concentrations produces dysfunction in the CNS mechanisms whose role is to regulate motor and sensory development and locomotor activity.

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Preliminary morphological and morphometric study of rat cerebellum following sodium arsenite exposure during rapid brain growth (RBG) period

Cited by 40 publications

References 44 publications

Taurine resumed neuronal differentiation in arsenite-treated N2a cells through reducing oxidative stress, endoplasmic reticulum stress, and mitochondrial dysfunction

Taurine resumed neuronal differentiation in arsenite-treated N2a cells through reducing oxidative stress, endoplasmic reticulum stress, and mitochondrial dysfunction

Scientific Opinion on Arsenic in Food

Locomotor activity and sensory – motor developmental alterations in rat offspring exposed to arsenic prenatally and via lactation

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