Effect of Sodium Thiosulfate on Isolated Cardiac Interfibrillar and Subsarcolemmal Mitochondria
Vascular Biology Lab, School of Chemical and Biotechnology, SASTRA University, Thanjavur-613 401, India
Vascular Biology Lab, School of Chemical and Biotechnology, SASTRA University, Thanjavur-613 401, India E-mail: firstname.lastname@example.org; email@example.com
Mitochondria are the key players of cardiac function and their dysfunction due to oxidative stress is implicated in myocardial ischemia reperfusion injury, one of the important mediators of cardiac mortality. The present study evaluates the mitochondrial protective effect of sodium thiosulfate on isolated cardiac mitochondria (interfibrillar mitochondria and subsarcolemmal mitochondria) subjected to oxidative stress by ischemia and reperfusion. Briefly, interfibrillar mitochondria and subsarcolemmal mitochondria were treated with cobalt chloride (500 µM) for 20 min to induce oxidative stress by chemical method and nitrogen gas purging for 20 min in an ischemic buffer was used for the physiological method. The mitoprotective effect of sodium thiosulfate was evaluated with different mode of sodium thiosulfate incubation (pretreatment, cotreatment and post treatment) with the mitochondria. The mitochondria led to an increased oxidative stress (measured by malondialdehyde, reduced glutathione, superoxide dismutase and glutathione peroxidase) and decreased mitochondrial enzyme activities (measured by succinate dehydrogenase, malate dehydrogenase and NAD+ dehydrogenase) with both the models and sodium thiosulfate treated groups showed significant improvement in the above alterations. By comparing the efficiency among the different modes of sodium thiosulfate treatment, we found that pretreatment renders significant (P<0.05) mitochondrial protection against ischemia reperfusion injury by nitrogen gas. However, no such differences were observed among the treatments in cobalt chloride mediated mitochondrial dysfunction. In summary, we found that sodium thiosulfate can modulate and preserve cardiac mitochondria for the treatment of myocardial ischemia reperfusion injury.