Thiol oxidative stress has been implicated in a variety of cardiovascular diseases including heart failure. Thiol redox state (TRS) is expressed as the ratio of thiols to disulfides within the cell.  Disulfides are reduced to their corresponding thiols by enzymes such as thioredoxin reductase (TrxR) and glutathione reducase (GR). Carvedilol is a �-blocker used to treat heart failure. It possesses antioxidant properties; however the exact mechanism of antioxidant effect is still unknown. H9c2 rat cardiomyocytes have been used as a model to demonstrate the protective effects of carvedilol against 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU) induced thiol oxidative stress. BCNU significantly increased protein disulfide content; however, a combination of carvedilol and BCNU was able to lower protein disulfide content to control levels after a 2 hour treatment. This was correlated with an increase in TrxR activity.  No change in GR activity was observed.  Carvedilol may protect against thiol oxidative stress via the thioredoxin pathway.

Carvedilol lowers protein disulfides via the thioredoxin pathway in thiol oxidative stress

248th National Meeting (2014)

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