Lei Tian1, Nan Chu2, Hu Yang3, Jun Yan4, Bencheng Lin5, Wei Zhang6, Kang Li7, Wenqing Lai8, Liping Bian9, Huanliang Liu10, Zhuge Xi11, Xiaohua Liu12. 1. Tianjin Institute of Environmental and Operational Medicine, No. 1 Dali Road, Heping District, Tianjin, 300050, China. Electronic address: tjtianei@126.com. 2. Affiliated Zhongshan Hospital of Dalian University, Dalian, 116001, China. Electronic address: chunan120@163.com. 3. Tianjin Institute of Environmental and Operational Medicine, No. 1 Dali Road, Heping District, Tianjin, 300050, China; Affiliated Zhongshan Hospital of Dalian University, Dalian, 116001, China. Electronic address: stancooper@163.com. 4. Tianjin Institute of Environmental and Operational Medicine, No. 1 Dali Road, Heping District, Tianjin, 300050, China. Electronic address: yanjying@sina.cn. 5. Tianjin Institute of Environmental and Operational Medicine, No. 1 Dali Road, Heping District, Tianjin, 300050, China. Electronic address: linbencheng123@126.com. 6. Tianjin Institute of Environmental and Operational Medicine, No. 1 Dali Road, Heping District, Tianjin, 300050, China. Electronic address: 15620001611@163.com. 7. Tianjin Institute of Environmental and Operational Medicine, No. 1 Dali Road, Heping District, Tianjin, 300050, China. Electronic address: tjlikang@126.com. 8. Tianjin Institute of Environmental and Operational Medicine, No. 1 Dali Road, Heping District, Tianjin, 300050, China. Electronic address: laiwenqing@126.com. 9. Tianjin Institute of Environmental and Operational Medicine, No. 1 Dali Road, Heping District, Tianjin, 300050, China. Electronic address: bmoglp@126.com. 10. Tianjin Institute of Environmental and Operational Medicine, No. 1 Dali Road, Heping District, Tianjin, 300050, China. Electronic address: tjliuhuanliang@126.com. 11. Tianjin Institute of Environmental and Operational Medicine, No. 1 Dali Road, Heping District, Tianjin, 300050, China. Electronic address: zhugexi2003@sina.com. 12. Tianjin Institute of Environmental and Operational Medicine, No. 1 Dali Road, Heping District, Tianjin, 300050, China. Electronic address: liuxiaohua1992@sina.com.
Abstract
OBJECTIVE: To clarify the cardiotoxicity induced by acute exposure to different concentrations of ozone in both gender rats and explore the underlying mechanisms. METHODS: A total of 240 rats were randomly sorted into 6 groups with equal numbers of male and female rats in each group. The rats were subjected to ozone inhalation at concentrations of 0, 0.12, 0.5, 1.0, 2.0 and 4.0 ppm, respectively, for 6 h. After ozone exposure, function indicators, myocardial injury indexes and risk factors of cardiovascular disease in blood were assayed. RESULTS: High ozone exposure resulted in sustained ventricular tachycardia in male and female rats. Myocardial apoptosis in male rats started from 1.0 ppm ozone, and that in female rats started from 2.0 ppm ozone (p < 0.05). Caspase-9 increased significantly from 0.12 ppm ozone (p < 0.01) in both gender rats, while caspase-3 was initially activated at 0.5 ppm ozone. From 1.0 ppm ozone, mitochondrial cristae and myofilaments dissolved. The ratio of Bcl-2/Bax decreased significantly from 0.12 ppm and MRCC-IV decreased significantly from 2.0 ppm by ozone. CONCLUSION: Acute ozone exposure can cause paroxysmal ventricular tachycardia in rats. Moreover, the changes of inflammatory factors in the heart tissues of female and male rats after ozone exposure were greater than those of oxidative stress. This study reported for the first time that 6 h ozone exposure does not cause acute cardiomyocyte necrosis, but promotes cardiomyocyte apoptosis in a mitochondrial-dependent manner. Ozone could regulate caspases-3 dependent cardiomyocyte apoptosis by affecting the balance between caspase-9 and XIAP.
OBJECTIVE: To clarify the cardiotoxicity induced by acute exposure to different concentrations of ozone in both gender rats and explore the underlying mechanisms. METHODS: A total of 240 rats were randomly sorted into 6 groups with equal numbers of male and female rats in each group. The rats were subjected to ozone inhalation at concentrations of 0, 0.12, 0.5, 1.0, 2.0 and 4.0 ppm, respectively, for 6 h. After ozone exposure, function indicators, myocardial injury indexes and risk factors of cardiovascular disease in blood were assayed. RESULTS: High ozone exposure resulted in sustained ventricular tachycardia in male and female rats. Myocardial apoptosis in male rats started from 1.0 ppm ozone, and that in female rats started from 2.0 ppm ozone (p < 0.05). Caspase-9 increased significantly from 0.12 ppm ozone (p < 0.01) in both gender rats, while caspase-3 was initially activated at 0.5 ppm ozone. From 1.0 ppm ozone, mitochondrial cristae and myofilaments dissolved. The ratio of Bcl-2/Bax decreased significantly from 0.12 ppm and MRCC-IV decreased significantly from 2.0 ppm by ozone. CONCLUSION: Acute ozone exposure can cause paroxysmal ventricular tachycardia in rats. Moreover, the changes of inflammatory factors in the heart tissues of female and male rats after ozone exposure were greater than those of oxidative stress. This study reported for the first time that 6 h ozone exposure does not cause acute cardiomyocyte necrosis, but promotes cardiomyocyte apoptosis in a mitochondrial-dependent manner. Ozone could regulate caspases-3 dependent cardiomyocyte apoptosis by affecting the balance between caspase-9 and XIAP.
Authors: Ziyi Liu; Fuxu Gong; Lei Tian; Jun Yan; Kang Li; Yizhe Tan; Jie Han; Yue Zhao; Da Li; Zhuge Xi; Xiaohua Liu Journal: Sports Med Health Sci Date: 2022-06-22