Arsenic exposure alters the expression of genes related to metabolic diseases in differentiated adipocytes and in newborns and children.

The mechanisms underlying the association between prenatal arsenic exposure and the development of metabolic diseases remain unclear. Aberrant adipogenesis and adipokine production are associated with increased risk for the development of metabolic diseases in susceptible populations. Generation of mature adipocytes is tightly regulated by the expression of genes encoding: peroxisome proliferator-activated receptor γ (PPARG), fatty acid-binding protein (FABP4), and glucose transporter-4 (SLC2A4), and adipokines such as leptin (LEP) and adiponectin (ADIPOQ).

arsenic exposure increases DNA damage and gene expression changes in umbilical cord mesenchymal stem cells (UC-MSCs) from newborns as well as in UC-MSC differentiated hepatocytes.

Prenatal exposure to arsenic is associated with an increased risk of disease development such as liver cancer in adulthood. Increasing evidence suggests that fetal stem cells are key targets during transplacental chemical exposure. Our earlier study reported that arsenic exposure caused various types of DNA damage in newborns.

Correction to: Exposure to arsenic in utero is associated with various types of DNA damage and micronuclei in newborns: a birth cohort study.

Following publication of the original article [1], the author reported that incorrect version of Tables 1, 3, 5 and 6 were published.

Exposure to arsenic in utero is associated with various types of DNA damage and micronuclei in newborns: a birth cohort study.

Background: Growing evidence indicates that in utero arsenic exposures in humans may increase the risk of adverse health effects and development of diseases later in life. This study aimed to evaluate potential health risks of in utero arsenic exposure on genetic damage in newborns in relation to maternal arsenic exposure.

Methods: A total of 205 pregnant women residing in arsenic-contaminated areas in Hanam province, Vietnam, were recruited.

Hypomethylation of inflammatory genes (COX2, EGR1, and SOCS3) and increased urinary 8-nitroguanine in arsenic-exposed newborns and children.

Early-life exposure to arsenic increases risk of developing a variety of non-malignant and malignant diseases. Arsenic-induced carcinogenesis may be mediated through epigenetic mechanisms and pathways leading to inflammation. Our previous study reported that prenatal arsenic exposure leads to increased mRNA expression of several genes related to inflammation, including COX2, EGR1, and SOCS3.

Arsenic projects in SE Asia.

Early life exposure to inorganic arsenic is associated with a wide range of malignant and chronic disease outcomes in humans. Prenatal arsenic exposure may give rise to adverse effects on child health and development as arsenic readily passes through the placenta in human beings. The impact of maternal arsenic exposure on fetal gene expression was conducted in pregnant women living in Southern Thailand.

Oxidative DNA damage and repair in children exposed to low levels of arsenic in utero and during early childhood: application of salivary and urinary biomarkers.

The present study aimed to assess arsenic exposure and its effect on oxidative DNA damage and repair in young children exposed in utero and continued to live in arsenic-contaminated areas. To address the need for biological specimens that can be acquired with minimal discomfort to children, we used non-invasive urinary and salivary-based assays for assessing arsenic exposure and early biological effects that have potentially serious health implications. Levels of arsenic in nails showed the greatest magnitude of difference between exposed and control groups, followed by arsenic concentrations in saliva and urine.

Effects of arsenic exposure on DNA methylation in cord blood samples from newborn babies and in a human lymphoblast cell line.

Background: Accumulating evidence indicates that in utero exposure to arsenic is associated with congenital defects and long-term disease consequences including cancers. Recent studies suggest that arsenic carcinogenesis results from epigenetic changes, particularly in DNA methylation. This study aimed to investigate DNA methylation changes as a result of arsenic exposure in utero and in vitro.