Grune T, Schönheit K, Blasig I, Siems W
Clinics of Physical Therapy and Rehabilitation, Medical Faculty (Charité), Berlin, Germany.
Cell Biochem Funct. 1994 Jun;12(2):143-7. doi: 10.1002/cbf.290120210.
4-Hydroxynonenal (HNE) degradation was investigated in isolated perfused rat hearts of the WKY and SHR strains before and after ischemia. HNE (10 mumoles l-1) were infused and the concentration of HNE in the effluent was determined. The rate of initial consumption was about 50 nmoles min-1 g-1 wet weight in hearts of both the WKY and SHR rats. In the WKY rat hearts, this rate of HNE degradation did not change during several minutes of HNE infusion and also remained constant during postischemic reperfusion. In the hearts of the SHR rats the HNE degradation rate declined within 5 min to 25 nmoles min-1 g-1 wet weight. Also during postischemic reperfusion, there was a lower HNE degradation rate in the SHR rat hearts than in the WKY rat hearts. The influence of hypertrophy on the rate of HNE degradation is discussed. It is suggested that the low degradation of the cytotoxic lipid peroxidation product, HNE, in hypertrophic hearts may contribute to reduced antioxidant defence in those hearts.
在缺血前后，对WKY和SHR品系的离体灌注大鼠心脏中4-羟基壬烯醛（HNE）的降解情况进行了研究。注入HNE（10微摩尔/升），并测定流出液中HNE的浓度。WKY和SHR大鼠心脏的初始消耗速率约为50纳摩尔/分钟/克湿重。在WKY大鼠心脏中，HNE降解速率在注入HNE的几分钟内没有变化，并且在缺血后再灌注期间也保持恒定。在SHR大鼠心脏中，HNE降解速率在5分钟内降至25纳摩尔/分钟/克湿重。同样在缺血后再灌注期间，SHR大鼠心脏中的HNE降解速率低于WKY大鼠心脏。讨论了肥大对HNE降解速率的影响。有人认为，肥大心脏中细胞毒性脂质过氧化产物HNE的低降解可能导致这些心脏中抗氧化防御能力降低。
