Publications by authors named "Somchamai Waraprasit"

Article Synopsis
  • Growing evidence indicates that arsenic exposure can lead to increased risks of chronic diseases and cancers linked to inflammation.
  • A previous study showed that arsenic-exposed newborns had higher inflammatory gene activity and DNA damage due to hypomethylation of gene promoters.
  • The current research demonstrates that methyl group donors like S-adenosyl methionine (SAM) and folic acid can reverse this hypomethylation, reduce inflammatory gene expression, and lower DNA damage markers in human cells, suggesting their potential as preventive measures against arsenic toxicity.
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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.

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Cholangiocarcinoma (CCA) is a severe cancer with poor prognosis. The aim of the present study was to explore the expression of argininosuccinate synthetase (ASS), as well as the possibility of using pegylated arginine deiminase (ADI-PEG20) for the treatment of CCA. ASS expression was determined in CCA specimens from 40 patients in Thailand.

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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.

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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.

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