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Mitochondrial H2O2 metabolism as central event of heart complex I syndrome in early diabetes

内科学 线粒体 内分泌学 链脲佐菌素 糖尿病 氧化应激 胰岛素 线粒体内膜 过氧化氢酶 过氧化脂质 脂质过氧化 线粒体ROS 化学 生物 医学 生物化学
作者
Ivana A. Rukavina-Mikusic,Micaela Rey,Juan Santiago Adán Areán,Virginia Vanasco,Silvia Álvarez,Laura B. Valdez
出处
期刊:Free Radical Biology and Medicine [Elsevier BV]
卷期号:201: 66-75 被引量:2
标识
DOI:10.1016/j.freeradbiomed.2023.03.011
摘要

Hydrogen peroxide is the main metabolite effective in redox regulation and it is considered an insulinomimetic agent, with insulin signalling being essential for normal mitochondrial function in cardiomyocytes. Therefore, the aim of this work was to deeply analyse the heart mitochondrial H2O2 metabolism, in the early stage of type 1 diabetes. Diabetes was induced by Streptozotocin (STZ, single dose, 60 mg × kg-1, ip.) in male Wistar rats and the animals were sacrificed 10 days after injection. Mitochondrial membrane potential and ATP production, using malate-glutamate as substrates, in the heart of diabetic animals were like the ones observed in control group. Mn-SOD activity was lower (15%) in the heart of diabetic rats even though its expression was increased (29%). The increment in heart mitochondrial H2O2 production (117%) in diabetic animals was accompanied by an enhancement in the activities and expressions of glutathione peroxidase (26% and 42%) and of catalase (200% and 133%), with no changes in the peroxiredoxin activity, leading to [H2O2]ss ∼40 nM. Heart mitochondrial lipid peroxidation and protein nitration were higher in STZ-injected animals (45% and 42%) than in control group. The mitochondrial membrane potential and ATP production preservation suggest the absence of irreversible damage at this early stage of diabetes 1. The increase in mitochondrial [H2O2]ss above the physiological range, but still below supraphysiological concentration (∼100 nM) seems to be part of the adaptive response triggered in cardiomyocytes due to the absence of insulin. The signs of mitochondrial dysfunction observed in this very early stage of diabetes are consistent with the mitochondrial entity called ″complex I syndrome″.
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