Abstract

Pyrrolidinedithiocarbamate (PDTC) and N-acetylcysteine (NAC) have been used as antioxidants to prevent apoptosis in lymphocytes, neurons, and vascular endothelial cells. We report here that PDTC and NAC induce apoptosis in rat and human smooth muscle cells. In rat aortic smooth muscle cells, PDTC induced cell shrinkage, chromatin condensation, and DNA strand breaks consistent with apoptosis. In addition, overexpression of Bcl-2 suppressed vascular smooth muscle cell death caused by PDTC and NAC. The viability of rat aortic smooth muscle cells decreased within 3 h of treatment with PDTC and was reduced to 30% at 12 h. The effect of PDTC and NAC on smooth muscle cells was not species specific because PDTC and NAC both caused dose-dependent reductions in viability in rat and human aortic smooth muscle cells. In contrast, neither PDTC nor NAC reduced viability in human aortic endothelial cells. The use of antioxidants to induce apoptosis in vascular smooth muscle cells may help prevent their proliferation in arteriosclerotic lesions.

Highlights

  • Apoptosis or programmed cell death is characterized by cell shrinkage, membrane blebbing, and chromatin condensation that culminate in cell fragmentation [1]

  • We report here that PDTC and NAC induce apoptosis in rat and human smooth muscle cells

  • We tested the effects of PDTC and NAC on vascular smooth muscle and endothelial cells and show that both agents, in dose ranges at which they are used as antioxidants, induced apoptosis in rat and human aortic smooth muscle cells but not in human aortic endothelial cells

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Summary

Introduction

Apoptosis or programmed cell death is characterized by cell shrinkage, membrane blebbing, and chromatin condensation that culminate in cell fragmentation [1]. We report here that PDTC and NAC induce apoptosis in rat and human smooth muscle cells. In rat aortic smooth muscle cells, PDTC induced cell shrinkage, chromatin condensation, and DNA strand breaks consistent with apoptosis.

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