How A Mutual Drug Causes Liver Failure

Acetaminophen (Tylenol)  kicks off widespread glutathionylation, researchers find

American Society for Biochemistry in addition to Molecular Biology

IMAGE: High doses of acetaminophen, also known every bit Tylenol, tin ship away harm the liver. This figure shows how acetaminophen (APAP) is broken downwardly into a reactive chemical compound (NAPQI) that binds covalently to... view more 

Credit: Chan et al., Molecular & Cellular Proteomics 2018

Acetaminophen is a mutual hurting reliever constitute inwards every pharmacy. However, it is also the No. 1 displace of astute liver failure inwards the United States. In the liver, acetaminophen is converted into a novel chemical compound that covalently binds to proteins at an amino acid called cysteine. These covalent binding events are known to contribute to the toxicity of acetaminophen, but they cannot fully trouble organisation human relationship for its role inwards liver failure. The chemical compound is known to impair the activeness of mitochondria, the cell's release energy supplier, but does non bind direct to only about of the enzymes inwards mitochondria whose activeness it affects. Now researchers receive got constitute a novel agency that the breakdown production affects proteins inwards the liver.
James Chun Yip Chan in addition to colleagues at the National University of Singapore examined glutathionylation, a post-translational change made to cysteine residues, inwards reply to acetaminophen toxicity. In a study published inwards the mag Molecular & Cellular Proteomics, the researchers reported a novel proteomic approach to isolate in addition to position glutathionylated proteins in addition to applied it inwards cells treated with acetaminophen. They constitute that an acetaminophen breakdown production tin ship away displace glutathionylation, suggesting a novel machinery for the harm the drug causes.
Usually, glutathione is added to cysteine residues to protect them from harm past times oxygen nether stressful conditions. Chan in addition to colleagues showed that acetaminophen in addition to its breakdown production activate glutathionylation inwards a dose-dependent way. The change affects proteins involved inwards mitochondrial fuel uptake in addition to release energy production, leading to metabolic dysfunction in addition to other effects linked to acetaminophen toxicity. This interrogation helps explicate the drug's toxicity at high doses, particularly with enzymes that are impaired past times acetaminophen handling without binding direct to the drug or its metabolites. The findings may also apply to other drugs with like structures.
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