The Role of Sulfur Dioxide in the Regulation of Mitochondrion-Related Cardiomyocyte Apoptosis in Rats with Isopropylarterenol-Induced Myocardial Injury

Abstract

The authors investigated the regulatory effects of sulfur dioxide (SO2) on myocardial injury induced by isopropylarterenol (ISO) hydrochloride and its mechanisms. Wistar rats were divided into four groups: control group, ISO group, ISO plus SO2 group, and SO2 only group. Cardiac function was measured and cardiomyocyte apoptosis was detected. Bcl-2, bax and cytochrome c (cytc) expressions, and caspase-9 and caspase-3 activities in the left ventricular tissues were examined in the rats. The opening status of myocardial mitochondrial permeability transition pore (MPTP) and membrane potential were analyzed. The results showed that ISO-treated rats developed heart dysfunction and cardiac injury. Furthermore, cardiomyocyte apoptosis in the left ventricular tissues was augmented, left ventricular tissue bcl-2 expression was down-regulated, bax expression was up-regulated, mitochondrial membrane potential was significantly reduced, MPTP opened, cytc release from mitochondrion into cytoplasm was significantly increased, and both caspase-9 and caspase-3 activities were increased. Administration of an SO2 donor, however, markedly improved heart function and relieved myocardial injury of the ISO-treated rats; it lessened cardiomyocyte apoptosis, up-regulated myocardial bcl-2, down-regulated bax expression, stimulated mitochondrial membrane potential, closed MPTP, and reduced cytc release as well as caspase-9 and caspase-3 activities in the left ventricular tissue. Hence, SO2 attenuated myocardial injury in association with the inhibition of apoptosis in myocardial tissues, and the bcl-2/cytc/caspase-9/caspase-3 pathway was possibly involved in this process.

Endogeous sulfur dioxide protects against oleic acid-induced acute lung injury in association with inhibition of oxidative stress in rats

“…It was found that SO 2 decreased cardiomyocyte apoptosis likely via stimulation of mitochondrial potential. 54 Clarifying detailed mechanisms by which SO 2 impacts the oxidative stress and apoptosis needs further studies.…”

Signal pathways involved in the biological effects of sulfur dioxide

“…opening (Jin et al, 2013a). SO 2 reduced cell apoptosis in rat myocardial injury induced by isoproterenol.…”

“…The results showed that SO 2 promoted Bcl-2 expression, inhibited the release of cyc from the mitochondrion into cytoplasm, inhibited Bax expression, and inhibited the activation of caspase-9 and caspase-3 in myocardial injury induced by isoproterenol. Thus, the Bcl-2/cytc/caspase-9/caspase-3 pathway was involved in isoproterenol-induced myocardial injury in rats (Jin et al, 2013a).…”

Component Determination and Their Formation of PM2.5

“…[54][55][56] The studies have shown that prolonged exposure to sulfur compounds can lead to respiratory and myocardial diseases. [57][58][59][60][61][62][63] On the other hand, the intensities of H − and CN − decreased along with the increase of sputtering time, and the intensities of O − and Cl − become stronger along with the increase of the depth (Fig. 7(b)).…”