作者: D. T. Lucas , L. I. Szweda
关键词:
摘要: Cardiac reperfusion and aging are associated with increased rates of mitochondrial free radical production. Mitochondria therefore a likely site reperfusion-induced oxidative damage, the severity which may increase age. 4-Hydroxy-2-nonenal (HNE), major product lipid peroxidation, increases in concentration upon ischemic cardiac tissue, can react inactivate enzymes, inhibits respiration vitro. HNE modification protein(s) might, therefore, be expected to occur during result loss function. In addition, this process more prevalent aged animals. To begin test hypothesis, hearts from 8- 24-month-old rats were perfused Langendorff fashion subjected periods ischemia and/or reperfusion. The rate state 3 mitochondria isolated exposed (25 min) was approximately 25% less than that controls, independent Reperfusion (40 caused further decline 24- but not 8-month-old rats. Furthermore, protein (∼30 44 kDa) occurred only Thus, HNE-modified present those exhibiting declines These studies identify as subcellular target damage age-related susceptibility injury.