Gestational exposure to mercury leads to persistent changes in T-cell phenotype and function in adult DBF<sub>1</sub>mice

Pilones, Karsten A.; Tatum, Arthur H.; Gavalchin, Jerrie

doi:10.1080/15476910903084021

Cited by 15 publications

(6 citation statements)

References 56 publications

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“…No recovery from vinyl chlorideinduced carcinogenicity in mice occurred after only 1 month of vinyl chloride exposure, with younger animals (2-months old) being even more susceptible than animals 6-or 12-months old at the initiation of exposure (Bhandari, 1983). Gestational-only exposure to mercury in mice has been shown to cause persistent immune dysregulation that last until adulthood (Pilones et al, 2009). Moderate prenatal alcohol exposure induced laterlife immune dysfunction in rats (Terasaki and Schwarz, 2016).…”

Section: Discussionmentioning

confidence: 99%

Exposure Cessation During Adulthood Did Not Prevent Immunotoxicity Caused by Developmental Exposure to Low-Level Trichloroethylene in Drinking Water

Gilbert

Bai

Barnette

et al. 2017

Toxicological Sciences

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Exposure to the water pollutant trichloroethylene (TCE) can promote autoimmunity in both humans and rodents. Using a mouse model we have shown that chronic adult exposure to TCE at 500 μg/ml in drinking water generates autoimmune hepatitis in female MRL+/+ mice. There is increasing evidence that developmental exposure to certain chemicals can be more toxic than adult exposure. This study was designed to test whether exposure to a much lower level of TCE (0.05 μg/ml) during gestation, lactation, and early life generated autoimmunity similar to that found following adult exposure to higher concentrations of TCE. When female MRL+/+ mice were examined at postnatal day (PND) 259 we found that developmental/early life exposure [gestational day 0 to PND 154] to TCE at a concentration 10 000 fold lower than that shown to be effective for adult exposure triggered autoimmune hepatitis. This effect was observed despite exposure cessation at PND 154. In concordance with the liver pathology, female MRL+/+ exposed during development and early life to TCE (0.05 or 500 μg/ml) generated a range of antiliver antibodies detected by Western blotting. Expression of proinflammatory cytokines by CD4+ T cells was also similarly observed at PND 259 in the TCE-exposed mice regardless of concentration. Thus, exposure to TCE at approximately environmental levels from gestational day 0 to PND 154 generated tissue pathology and CD4+ T cell alterations that required higher concentrations if exposure was limited to adulthood. TCE exposure cessation at PND 154 did not prevent the immunotoxicity.

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Section: Discussionmentioning

confidence: 99%

Exposure Cessation During Adulthood Did Not Prevent Immunotoxicity Caused by Developmental Exposure to Low-Level Trichloroethylene in Drinking Water

Gilbert

Bai

Barnette

et al. 2017

Toxicological Sciences

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“…Gestational Cd exposure has effects on behavior (Dési et al 1998) and on indicators of semen quality of offspring at adulthood (Petrochelli Banzato et al 2012). Likewise, chronic maternal exposure to Hg caused altered immune and neurologic functions (Pilones et al 2009) and behavioral effects (Onishchenko et al 2007) in offspring.…”

Section: Introductionmentioning

confidence: 99%

Effects of Periconception Cadmium and Mercury Co-Administration to Mice on Indices of Chronic Diseases in Male Offspring at Maturity

Çamsarı

Folger

McGee

et al. 2017

Environ Health Perspect

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Background:Long-term exposure to the heavy metals cadmium (Cd) and mercury (Hg) is known to increase the risk of chronic diseases. However, to our knowledge, exposure to Cd and Hg beginning at the periconception period has not been studied to date.Objective:We examined the effect of Cd and Hg that were co-administered during early development on indices of chronic diseases in adult male mice.Methods:Adult female CD1 mice were subcutaneously administered a combination of cadmium chloride (CdCl2) and methylmercury (II) chloride (CH3HgCl) (0, 0.125, 0.5, or 2.0 mg/kg body weight each) 4 days before and 4 days after conception (8 days total). Indices of anxiety-like behavior, glucose homeostasis, endocrine and molecular markers of insulin resistance, and organ weights were examined in adult male offspring.Results:Increased anxiety-like behavior, impaired glucose homeostasis, and higher body weight and abdominal adipose tissue weight were observed in male offspring of treated females compared with controls. Significantly increased serum leptin and insulin concentrations and impaired insulin tolerance in the male offspring of dams treated with 2.0 mg/kg body weight of Cd and Hg suggested insulin resistance. Altered mRNA abundance for genes associated with glucose and lipid homeostasis (GLUT4, IRS1, FASN, ACACA, FATP2, CD36, and G6PC) in liver and abdominal adipose tissues as well as increased IRS1 phosphorylation in liver (Ser 307) provided further evidence of insulin resistance.Conclusions:Results suggest that the co-administration of Cd and Hg to female mice during the early development of their offspring (the periconception period) was associated with anxiety-like behavior, altered glucose metabolism, and insulin resistance in male offspring at adulthood.Citation:Camsari C, Folger JK, McGee D, Bursian SJ, Wang H, Knott JG, Smith GW. 2017. Effects of periconception cadmium and mercury co-administration to mice on indices of chronic diseases in male offspring at maturity. Environ Health Perspect 125:643–650; http://dx.doi.org/10.1289/EHP481

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“…50–54 TCDD increased the expression of inflammatory cytokines, mucin 5AC and several matrix metalloproteinases (MMPs) in lungs of mice. 55 Exposure to mercury vapour or mercury ions causes direct airway irritation.…”

Section: Discussionmentioning

confidence: 99%

Identification of a unique gene expression signature in mercury and 2,3,7,8-tetrachlorodibenzo-p-dioxin co-exposed cells

et al. 2017

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Mercury (Hg) and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are major environmental contaminants that commonly co-occur in the environment. Both Hg and TCDD are associated with a number of human diseases including cancers. While the individual toxicological effects of Hg and TCDD have been extensively investigated, studies on co-exposure are limited to a few genes and pathways. Therefore, a significant knowledge gap exists in the understanding of the deleterious effects of co-exposure to Hg and TCDD. Due to the prevalence of Hg and TCDD co-contamination in the environment and the major human health hazards they pose, it is important to obtain a fuller understanding of genome-wide effects of Hg and TCDD co-exposure. In this study, by performing a comprehensive transcriptomic analysis of human bronchial epithelial cells (BEAS-2B) exposed to Hg and TCDD individually and in combination, we have uncovered a subset of genes with altered expression only in the co-exposed cells. We also identified the additive as well as antagonistic effects of Hg and TCDD on gene expression. Moreover, we found that co-exposure impacted several biological and disease processes not affected by Hg or TCDD individually. Our studies show that the consequences of Hg and TCDD co-exposure on the transcriptional program and biological processes could be substantially different from single exposures, thus providing new insights into the co-exposure-specific pathogenic processes.

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Gestational exposure to mercury leads to persistent changes in T-cell phenotype and function in adult DBF₁mice

Cited by 15 publications

References 56 publications

Exposure Cessation During Adulthood Did Not Prevent Immunotoxicity Caused by Developmental Exposure to Low-Level Trichloroethylene in Drinking Water

Exposure Cessation During Adulthood Did Not Prevent Immunotoxicity Caused by Developmental Exposure to Low-Level Trichloroethylene in Drinking Water

Effects of Periconception Cadmium and Mercury Co-Administration to Mice on Indices of Chronic Diseases in Male Offspring at Maturity

Identification of a unique gene expression signature in mercury and 2,3,7,8-tetrachlorodibenzo-p-dioxin co-exposed cells

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Gestational exposure to mercury leads to persistent changes in T-cell phenotype and function in adult DBF1mice

Cited by 15 publications

References 56 publications

Exposure Cessation During Adulthood Did Not Prevent Immunotoxicity Caused by Developmental Exposure to Low-Level Trichloroethylene in Drinking Water

Exposure Cessation During Adulthood Did Not Prevent Immunotoxicity Caused by Developmental Exposure to Low-Level Trichloroethylene in Drinking Water

Effects of Periconception Cadmium and Mercury Co-Administration to Mice on Indices of Chronic Diseases in Male Offspring at Maturity

Identification of a unique gene expression signature in mercury and 2,3,7,8-tetrachlorodibenzo-p-dioxin co-exposed cells

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Gestational exposure to mercury leads to persistent changes in T-cell phenotype and function in adult DBF₁mice