Comparative effects of single intraperitoneal or oral doses of sodium arsenate or arsenic trioxide during in utero development

Stump, Donald G.; Holson, Joseph F.; Fleeman, T.L.; Nemec, M.D.; Farr, Craig H.

doi:10.1002/(sici)1096-9926(199911)60:5<283::aid-tera9>3.0.co;2-7

Cited by 42 publications

(26 citation statements)

References 15 publications

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“…While the prevalence of decreased body weight and growth was higher in boys, the effect was more marked in girls (Saha et al, 2012). Adverse effect on body weight due to arsenic exposure in experimental studies was irrespective of time and dose in most of the studies (Stump et al, 1999; Ekong et al, 2012). Loss of body weight following early life exposure to arsenic at low dose as observed in the present study indicates growth impairment and exhibit vulnerability of developing rats to the toxic effects of arsenic and is consistent with earlier experimental reports (Dhar et al, 2005; Bashir et al, 2006).…”

Section: Discussionmentioning

confidence: 98%

“…Enhanced oxidative stress associated with increased apoptosis was found to be linked to arsenic induced neurotoxicity (Estus et al, 1994;Namgung and Xia, 2001;Ahmed et al, 2011Ahmed et al, , 2012. Arsenic has been found to cross the placental barrier and cause developmental abnormalities including malformations, decreased growth rate, mortality and neural tube defects (Golub, 1994;Tabocova et al, 1996;Stump et al, 1999). In view of increasing risk of exposure to arsenic and associated vulnerabilities of the developing brain, studies have been carried out to assess the impact of arsenic exposure during prenatal and early post-natal periods (Anderson et al, 2000;Xi et al, 2010a;Lu et al, 2012;Herrera et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

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Reversibility of changes in brain cholinergic receptors and acetylcholinesterase activity in rats following early life arsenic exposure

Chandravanshi

Yadav

Shukla

et al. 2014

Intl J of Devlp Neuroscience

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In view of the increasing incidences of arsenic induced health effects and the vulnerability of the developing brain to its toxic effects, studies have been carried out to investigate the mechanism of arsenic induced cholinergic alterations and understand if such changes are persistent or transient on withdrawal of arsenic exposure. Male rats were exposed to arsenic (2 mg/kg or 4 mg/kg body weight, p.o) from post-lactational day (PD)22 to PD59, and the effect on selected behavioral and neurochemical end points associated with cholinergic functions was assessed on PD60 and PD90. Decrease in the binding of muscarinic-cholinergic receptors in frontal cortex (26%, 43%) and hippocampus (21%, 34%) associated with reduced CHRM2 mRNA levels, acetylcholinesterase activity and expression of ChAT and PKC β-1 was observed in arsenic exposed rats on PD60 as compared to controls. Spatial learning and memory and muscle strength were affected following arsenic exposure in rats on PD60 and associated with arsenic induced cholinergic alterations. Enhanced oxidative stress associated with increased expression of pro-apoptotic proteins and decreased expression of anti-apoptotic proteins was distinct in both frontal cortex and hippocampus following arsenic exposure in rats on PD60. The cholinergic alterations and other neurochemical modifications were found to be linked with increased arsenic levels in frontal cortex (1.39, 3.90-fold) and hippocampus (3.23, 5.48-fold) on PD60. Although a trend of recovery was observed both in behavioral and neurochemical endpoints on withdrawal of arsenic exposure on PD90, the results indicate that continuous arsenic exposure may have detrimental effects.

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Section: Discussionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Reversibility of changes in brain cholinergic receptors and acetylcholinesterase activity in rats following early life arsenic exposure

Chandravanshi

Yadav

Shukla

et al. 2014

Intl J of Devlp Neuroscience

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“…Wlodarczyk et al, 2001;B. J. Wlodarczyk, Bennett, Calvin, & Finnell, 1996); others reported no teratogenesis (Holson, Stump, Ulrich, & Farr, 1999;Nemec, Holson, Farr, & Hood, 1998;Stump, Holson, Fleeman, Nemec, & Farr, 1999). Few studies reported OFCs among offspring (Burk & Beaudoin, 1977;Ferm et al, 1971;Hood et al, 1982;Rogers et al, 1981).…”

Section: Introductionmentioning

confidence: 99%

“…Similar to human studies for arsenic‐contaminated drinking water, animal studies that examined the developmental toxicity of arsenic are equivocal. Several studies reported embryotoxic effects and occurrence of birth defects in offspring following maternal prenatal exposure to inorganic arsenic (Beaudoin, ; Burk & Beaudoin, ; Ferm, Saxon, & Smith, ; Hood & Bishop, ; Hood, Harrison, & Vedel, ; Morrissey & Mottet, ; Rogers, Chernoff, & Kavlock, ; B. Wlodarczyk et al, ; B. J. Wlodarczyk, Bennett, Calvin, & Finnell, ); others reported no teratogenesis (Holson, Stump, Ulrich, & Farr, ; Nemec, Holson, Farr, & Hood, ; Stump, Holson, Fleeman, Nemec, & Farr, ). Few studies reported OFCs among offspring (Burk & Beaudoin, ; Ferm et al, ; Hood et al, ; Rogers et al, ).…”

Section: Introductionmentioning

confidence: 99%

Maternal arsenic exposure and nonsyndromic orofacial clefts

Suhl

Leonard

Weyer

et al. 2018

Birth Defects Research

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Background: Arsenic is widely distributed in the environment in both inorganic and organic forms. Evidence from animal studies suggests that maternal inorganic arsenic may lead to the development of orofacial clefts (OFC)s in offspring. This evidence, together with the limited epidemiologic data available, supports the need for a comprehensive examination of major sources of arsenic exposure and OFCs in humans. Methods: Using interview data collected in the National Birth Defects Prevention Study, public and well water arsenic sampling data, and dietary arsenic estimates, we compared expert-rater assessed occupational arsenic exposure, individual-level exposure to arsenic through drinking water, and dietary arsenic exposure between mothers of OFC cases (N = 435) and unaffected controls (N = 1267). Associations for each source of exposure were estimated for cleft lip ± palate (CL/P) and cleft palate (CP) using unconditional logistic regression analyses. Results: Associations for maternal drinking water arsenic exposure and CL/P were near or below unity, whereas those for dietary arsenic exposure tended to be positive. For CP, positive associations were observed for maternal occupational arsenic and inorganic arsenic exposures, with confidence intervals that excluded the null value, whereas those for drinking water or dietary arsenic exposures tended to be near or below unity. Conclusions: Positive associations were observed for maternal occupational arsenic exposure and CP and for maternal dietary arsenic exposure and CL/P; the remainder of associations estimated tended to be near or below unity. Given the exploratory nature of our study, the results should be interpreted cautiously, and continued research using improved exposure assessment methodologies is recommended.

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“…Both inorganic and methylated arsenic injections caused developmental toxicity at maternally toxic or near lethal doses. In contrast, single or repeated oral exposure to inorganic arsenic did not induce fetal gross malformation in mice or rats (Holson et al 2000b;Stump et al 1998aStump et al , 1999. At maternally toxic doses, repeated oral exposures to dimethylarsinic acid increased resorptions and decreased fetal weight in mice and rats (Rogers, Chernoff, and Kavlock 1981).…”

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confidence: 99%

Reproductive and Developmental Toxicity of Arsenic in Rodents: A Review

et al. 2006

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Arsenic is a recognized reproductive toxicant in humans and induces malformations, especially neural tube defects, in laboratory animals. Early studies showed that murine malformations occurred only when a high dose of inorganic arsenic was given by intravenous or intraperitoneal injection in early gestation. Oral gavage of inorganic arsenic at maternally toxic doses caused reduced fetal body weight and increased resorptions. Recently, arsenic reproductive and developmental toxicity has been studied in situations more similar to human exposures and using broader endpoints, such as behavioral changes and gene expression. For the general population, exposure to arsenic is mostly oral, particularly via drinking water, repeated and prolonged over time. In mice and rats, methylated or inorganic arsenic via drinking water or by repeated oral gavage induced male and female reproductive and developmental toxicities. Furthermore, at nonmaternally toxic levels, inorganic arsenic given to pregnant dams via drinking water affected fetal brain development and postnatal behaviors. However, arsenic given by repeated oral gavage to pregnant mice and rats was not morphologically teratogenic. In this review of arsenic reproductive and developmental toxicity in rats and mice, the authors summarize recent in vivo studies and discuss possible underlying mechanisms. The influences of folate, selenium, zinc, and arsenic methylation on arsenic reproductive and developmental toxicity are also discussed.

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Comparative effects of single intraperitoneal or oral doses of sodium arsenate or arsenic trioxide during in utero development

Cited by 42 publications

References 15 publications

Reversibility of changes in brain cholinergic receptors and acetylcholinesterase activity in rats following early life arsenic exposure

Reversibility of changes in brain cholinergic receptors and acetylcholinesterase activity in rats following early life arsenic exposure

Maternal arsenic exposure and nonsyndromic orofacial clefts

Reproductive and Developmental Toxicity of Arsenic in Rodents: A Review

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