The thioredoxin system as a target for mercury compounds

Conclusions.The mechanism of toxicity for mercurials is a complex chain of events starting with inhibition of the selenoenzyme, thioredoxin reductase (TrxR). Selenium supplementation protects TrxR from the toxicity of inorganic forms of mercury (i.e.Hg(II)) to a certain extent, but not from methylmercury.When TrxR is inhibited, thioredoxin is reduced by alternative mechanisms involving glutathione and glutaredoxin and only when this pathway is hampered does cell death occur.General Significance.The understanding of the molecular mechanism of mercury toxicity and mechanisms of enzymatic compensation allows the design of mitigation strategies and, since TxrR and Trx exist in the plasma, puts forward the possibility for future use of changes in activity/expression of these enzymes as biomarkers of mercury toxicity, thus refining the risk assessment process.
Source: Biochimica et Biophysica Acta (BBA) General Subjects - Category: Biochemistry Source Type: research