Sodium tanshinone IIA sulfonate mediates electron transfer reaction in rat heart mitochondria

Authors

Guangyin Zhou, Institute of Biophysics
Wen Jiang, Institute of Biophysics
Yan Zhao, Institute of Biophysics
Guangén Ma, The National Institute of Pharmaceutical Research and Development
Wenjuan Xin, Institute of Biophysics
Junjie Yin, CFSAN
Baolu Zhao, Institute of Biophysics

Date of this Version

2003

Comments

Published in Biochemical Pharmacology 65 (2003) 51-57.

Abstract

In this paper, an electron transfer reaction mediated by sodium tanshinone IIA sulfonate (STS) was studied in rat heart mitochondria. It was found that STS could stimulate mitochondrial NADH oxidation dose-dependently and partly restore NADH oxidation in the presence of respiratory inhibitor (rotenone or antimycin A or KCN). It was likely that STS could accept electrons from complex I similar to ferricyanide and could be converted to its semiquinone form that could then reduce oxygen molecule. The data also showed that cytochrome c (Cyt c) could be reduced by STS in the presence of KCN, or STS could transfer the electron to oxygen directly. Free radicals were involved in the process. The results suggest that STS may protect ischemia-reperfusion injury through an electron transfer reaction in mitochondria against forming reactive oxygen radicals.