1Department of Biochemistry, Cairo University, Egypt
2Department of Physiology, College of Medicine, Inje University Korea
3Department of Biochemistry, King Abdulaziz University, Saudi Arabia
4Department of Medical Biochemistry and Molecular Biology, Aswan University, Egypt
5Department of Internal Medicine and Nephrology, Aswan University, Egypt
*Corresponding author: Jin Han, National Research Laboratory for Mitochondrial Signaling, Department of Physiology, College of Medicine, Cardiovascular and Metabolic Disease Center, Inje University 633-165 Gaegeum-Dong, Busanjin-Gu, Busan 613-735, Korea
Submission: February 09, 2018; Published: February 22, 2018
ISSN: 2578-0263Volume1 Issue2
Many data has accumulated supporting the involvement of oxidative stress in the development of diabetic cardiomyopathy. The current study was carried out to investigate the effect of diabetic oxidative stress on cardiac mitochondrial functions to figure out potential biomarkers and therapeutic targets for early diagnosis and treatment of diabetic cardiomyopathy. For this purpose, a total number of 18 male Otsuka Long-Evans Tokushima Fatty (OLETF) rats as diabetic group and age-matched Long–Evans Tokushima Otsuka (LETO) as control group were used in the present study.
Rats (both LETO and OLETF) were anesthetized and thoracotomy was performed, and hearts were per-fused. Furthermore, for mitochondrial isolation 12 hearts were used (6 for flow cytometry and another 6 for measurement of oxygen consumption). Additionally, to carry out DNA fragmentation assay and 8-OHdG measurement, 6 hearts were used for mitochondrial DNA extraction.
The obtained findings can be summarized in that electron microscopy of mitochondria from diabetic OLETF hearts revealed increases in both size and number. Moreover, mitochondrial DNA fragmentation percentage and oxidized mitochondrial DNA were higher in diabetic hearts when compared with control group, and demonstrated impaired mitochondrial function in diabetic group. In addition, data showed decrease in ETC respiration as measured by the alteration in respiratory control ratio (RCR) of diabetic OLETF heart mitochondria. It can be concluded that mitochondrial ROS are involved in the progression of diabetic cardiomyopathy. This can be explained in the light of the progression of mitochondrial dysfunction and increasing level of oxidative stress during diabetes in cardiac tissue.
Keywords: Mitochondria, Diabetes mellitus, Cardiac myocytes, obesity, oxidative stres