Keatisuwan W
Physiology Section, Hokkaido University, Sapporo, Japan.
Hokkaido Igaku Zasshi. 1992 Jul;67(4):488-97.
Alterations in phospholipids and phospholipase A2 activity produced in cardiac mitochondria and microsomes by prolonged exercise and the effect of quinacrine on these changes have been studied in two types of experiment done on rats subjected to prolonged swimming exercise. In Experiment I, rats swam for 0.5, 1.5 or 3 h carrying a weight representing 3% of body weight. At the end of exercise or after varying recovery periods, the hearts were removed, mitochondria and microsomes were isolated and phospholipid constituents, cholesterol and phospholipase A2 (PLA2) determined. The phosphatidylethanolamine (PE) and phosphatidylcholine (PC) levels in mitochondria were progressively reduced by exercise for 0.5, 1.5, and 3 h as compared with control rats (the rats which trained to swim with loading for 4 days and took rest for 1 night). After recovery periods of 6 and 12 h, levels were partially restored, but after 24 and 48 h they decreased slightly below the control values. By 120-240 h, PE and PC levels recovered to slightly higher values than control. In microsomes, PE and PC levels were also decreased at the end of exercise for 0.5, 1.5, or 3 h, but over recovery periods of 6 to 48 h, they gradually increased and stabilized. In Experiment II designed to study the cause of the exercise-induced decrease in PE and PC, intravenous quinacrine was used to inhibit PLA2. PE and PC in exercised rats injected with saline (ES group) were markedly decreased after prolonged exercise when compared with control rats injected with saline (CS group). In exercise rats injected with quinacrine (EQ group), PC was significantly decreased when compared with the CS group while PE was slightly decreased but was not significantly different. Total activity (TA) and specific activity (SA) of PLA2 in mitochondria did not differ significantly in the three groups. In microsomes, TA in the ES group was significantly increased compared with the CS group while that in EQ group was slightly increased but was not significantly different. SA was unchanged in three groups. These results suggest that quinacrine can partially prevent the decrease of phospholipid and partially inhibit the activity of PLA2 after prolonged exercise. RCR in ES group increased significantly after prolonged exercise while RCR in EQ group tended to increase. ADP/O ratio was not significantly different in all groups.
在对进行长时间游泳运动的大鼠所做的两类实验中,研究了长时间运动对心脏线粒体和微粒体中磷脂及磷脂酶A2活性的影响,以及奎纳克林对这些变化的作用。在实验I中,大鼠负重相当于体重3%的重物游泳0.5、1.5或3小时。运动结束时或经过不同的恢复期后,取出心脏,分离线粒体和微粒体,并测定磷脂成分、胆固醇和磷脂酶A2(PLA2)。与对照大鼠(经4天负重游泳训练并休息1晚的大鼠)相比,运动0.5、1.5和3小时后,线粒体中的磷脂酰乙醇胺(PE)和磷脂酰胆碱(PC)水平逐渐降低。在6小时和12小时的恢复期后,水平部分恢复,但在24小时和48小时后,它们略低于对照值。到120 - 240小时,PE和PC水平恢复到略高于对照的值。在微粒体中,运动0.5、1.5或3小时结束时,PE和PC水平也降低,但在6至48小时的恢复期内,它们逐渐升高并稳定下来。在旨在研究运动诱导的PE和PC降低原因的实验II中,静脉注射奎纳克林以抑制PLA2。与注射生理盐水的对照大鼠(CS组)相比,长时间运动后,注射生理盐水的运动大鼠(ES组)中的PE和PC显著降低。与CS组相比,注射奎纳克林的运动大鼠(EQ组)中的PC显著降低,而PE略有降低但无显著差异。三组中线粒体中PLA2的总活性(TA)和比活性(SA)无显著差异。在微粒体中,ES组的TA与CS组相比显著增加,而EQ组的TA略有增加但无显著差异。三组中的SA均未改变。这些结果表明,长时间运动后,奎纳克林可部分防止磷脂减少并部分抑制PLA2的活性。长时间运动后,ES组的呼吸控制率(RCR)显著增加,而EQ组的RCR有增加趋势。所有组中的ADP/O比值无显著差异。