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Selenomethionine administration decreases the oxidative stress induced by post mortem ischemia in the heart, liver and kidneys of rats
Biometals ( IF 3.5 ) Pub Date : 2021-04-28 , DOI: 10.1007/s10534-021-00310-3
Paul E Hasuoka 1 , Juan P Iglesias 2 , Mauricio Teves 2 , Marcos M Kaplan 2 , Nelson H Ferrúa 2 , Pablo H Pacheco 1
Affiliation  

Selenium is an essential element in human and animal metabolism integrated into the catalytic site of glutathione peroxidase (GPX1), an antioxidant enzyme that protects cells from damage caused by reactive oxygen species (ROS). Oxidative stress refers the imbalance between ROS and antioxidant defense systems. It generates alterations of DNA, proteins and lipid peroxidation. The imbalance occurs particularly during ischemia and lack of postmortem perfusion. This mechanism is of relevance in transplant organs, affecting their survival. The aim of this research is to evaluate the effect of seleno-methionine (SeMet) as a protective agent against postmortem ischemia injury in transplant organs. Wistar rats were orally administered with SeMet. After sacrifice, liver, heart and kidney samples were collected at different postmortem intervals (PMIs). SeMet administration produced a significant increase of Se concentration in the liver (65%, p < 0.001), heart (40%, p < 0.01) and kidneys (45%, p < 0.05). Levels of the oxidative stress marker malondialdehyde (MDA) decreased significantly compared to control in the heart (0.21 ± 0.04 vs. 0.12 ± 0.02 mmol g−1) and kidneys (0.41 ± 0.02 vs. 0.24 ± 0.03 mmol g−1) in a PMI of 1–12 h (p < 0.01). After SeMet administration for 21 days, a significant increase in GPX1 activity was observed in the liver (80%, p < 0.001), kidneys (74%, p < 0.01) and heart (35%, p < 0.05). SeMet administration to rats significantly decreased the oxidative stress in the heart, liver and kidneys of rats generated by postmortem ischemia.



中文翻译:

硒代蛋氨酸给药可降低死后缺血引起的大鼠心脏、肝脏和肾脏的氧化应激

硒是人类和动物新陈代谢中必不可少的元素,整合到谷胱甘肽过氧化物酶 (GPX1) 的催化位点中,GPX1 是一种抗氧化酶,可保护细胞免受活性氧 (ROS) 造成的损害。氧化应激是指活性氧和抗氧化防御系统之间的不平衡。它会产生 DNA、蛋白质和脂质过氧化的改变。这种不平衡尤其发生在缺血和缺乏死后灌注期间。这种机制与移植器官相关,影响它们的存活。本研究的目的是评估硒代蛋氨酸 (SeMet) 作为移植器官死后缺血损伤的保护剂的作用。Wistar 大鼠口服 SeMet。处死后,在不同的死后间隔 (PMI) 收集肝脏、心脏和肾脏样本。SeMet 给药使肝脏 (65%, p < 0.001)、心脏 (40%, p < 0.01) 和肾脏 (45%, p < 0.05) 中的硒浓度显着增加。与心脏中的对照相比,氧化应激标志物丙二醛 (MDA) 的水平显着下降(0.21 ± 0.04 对 0.12 ± 0.02 mmol g-1 ) 和肾脏 (0.41 ± 0.02 vs. 0.24 ± 0.03 mmol g -1 ) 在 1-12 小时的 PMI (p < 0.01)。SeMet 给药 21 天后,在肝脏 (80%, p < 0.001)、肾脏 (74%, p < 0.01) 和心脏 (35%, p < 0.05) 中观察到 GPX1 活性显着增加。SeMet 对大鼠的给药显着降低了死后缺血产生的大鼠心脏、肝脏和肾脏的氧化应激。

更新日期:2021-04-29
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