Acetaminophen

(Tylenol) A common, over-the-counter drug used to reduce fever and relieve mild to moderate pain, but which does not reduce redness or inflammation. – Harvard Dictionary of Health Terms, Harvard Medical Publishing

Abstract

Emerging research suggests that the timing of environmental factors in the presence of genetic predispositions has influenced the increase in autism spectrum disorders over the past several decades. A review of the medical literature suggests that autism may be impacted by environmental toxicants, breastfeeding duration, gut flora composition, nutritional status, acetaminophen use, vaccine practices and use of antibiotics and/or frequency of infections. The author reports her retrospective clinical research in a general pediatric practice (Advocates for Children), which shows a modest trend toward lower prevalence of autism than her previous pediatric practice or recent CDC data. Out of 294 general pediatrics patients followed since 2005 there were zero new cases of autism (p value 0.014). Given the prevalence of autism for that cohort of 1 in 50 children in the United States, it is important to consider implementing strategies in primary care practice that could potentially modify environmental factors or affect the timing of environmental triggers contributing to autism.

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  • July 30, 2013

Excerpt:
“We propose that children with the autism diagnosis are especially vulnerable to toxic metals such as aluminum and mercury due to insufficient serum sulfate and glutathione. A strong correlation between autism and the MMR (Measles, Mumps, Rubella) vaccine is also observed, which may be partially explained via an increased sensitivity to acetaminophen administered to control fever.”

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  • November 7, 2012

Abstract

Mercury toxicity is a highly interesting topic in biomedicine due to the severe endpoints and treatment limitations. Selenite serves as an antagonist of mercury toxicity, but the molecular mechanism of detoxification is not clear. Inhibition of the selenoenzyme thioredoxin reductase (TrxR) is a suggested mechanism of toxicity. Here, we demonstrated enhanced inhibition of activity by inorganic and organic mercury compounds in NADPH-reduced TrxR, consistent with binding of mercury also to the active site selenolthiol. On treatment with 5 μM selenite and NADPH, TrxR inactivated by HgCl(2) displayed almost full recovery of activity. Structural analysis indicated that mercury was complexed with TrxR, but enzyme-generated selenide removed mercury as mercury selenide, regenerating the active site selenocysteine and cysteine residues required for activity. The antagonistic effects on TrxR inhibition were extended to endogenous antioxidants, such as GSH, and clinically used exogenous chelating agents BAL, DMPS, DMSA, and α-lipoic acid. Consistent with the in vitro results, recovery of TrxR activity and cell viability by selenite was observed in HgCl(2)-treated HEK 293 cells. These results stress the role of TrxR as a target of mercurials and provide the mechanism of selenite as a detoxification agent for mercury poisoning.

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  • September 1, 2010