Why the study?
Does glutathione or N-acetylcysteine prevent doxorubicin-induced cardiotoxicity in rat models?
Does glutathione or N-acetylcysteine prevent doxorubicin-induced cardiotoxicity in rat models?
Intravenous glutathione, but not oral N-acetylcysteine, prevents doxorubicin-induced cardiotoxicity in vivo, highlighting the potential role of pharmacokinetic factors in cardioprotection.
Answers are grounded in this paper and cite their sources.
Should not change doxorubicin use in patients; leaves open whether IV GSH offers clinical cardioprotection.
The effects of two sulfhydryl compounds, glutathione (GSH) and N-acetylcysteine (NAC), on the cardiotoxicity of doxorubicin (DXR) were tested on in vitro and in vivo models. DXR was administered to rats as 4 weekly i.v. doses of 3 mg/kg. GSH (1.5 mmoles/kg), given i.v. 10 min before and 1 hr after DXR, was found to prevent the development of the delayed cardiotoxic effects of DXR, as assessed by electrocardiographic and mechanical parameters, as well as by histological examination of left ventricular preparations. In contrast, equimolar oral doses of NAC (1 hr before and 2 hrs after DXR) were found to be ineffective. Both GSH and NAC prevented the negative inotropic effect produced by DXR on isolated rat atria. A good correlation exists between the cardioprotective effects of the two agents and their ability to enhance the non-protein sulfhydryl group content of the myocardium. Differences observed in vivo between GSH and NAC might be accounted for by pharmacokinetic factors.
No takes yet. Share an insight, caveat, or question.
Villani et al. (1990) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: