Chan P H, Chen S, Fishman R A
Brain Edema Research Center, Department of Neurology, University of California, School of Medicine, San Francisco, CA 94143, U.S.A.
Neurochem Int. 1987;10(3):303-10. doi: 10.1016/0197-0186(87)90104-5.
Rat brain membranes were incubated with bee venom phospholipase A(2) (PLA(2)) or phospholipase C (PLC) from Clostridium perfringens. PLA(2) caused a significant increase in free polyunsaturated fatty acids concomitant with membrane phospholipid degradation as monitored by HPLC and by gas chromatography. Equal concentrations of PLC had a much lesser effect than PLA(2). Divergent and differential effects were shown on deacylation and incorporation of [(3)H]arachidonic acid in membrane phospholipids. The incorporation of [(3)H]arachidonic acid into various phospholipids was greatly reduced by PLA(2) (0.018 units/ml) whereas PLC at identical concentration was not effective. PLA(2) inhibited (Na(+) + K(+))-ATPase but was not effective on p-nitrophenyl-phosphatase activity whereas PLC stimulated both enzymes. PLA(2) induced swelling of cortical brain slices whereas PLC was not effective. Thus, the severity of the perturbation of membrane integrity, and the inhibition of (Na(+) + K(+))-ATPase in brain membranes may play an important role in cellular swelling of brain slices induced by PLA(2).
将大鼠脑膜与蜂毒磷脂酶A(2)(PLA(2))或产气荚膜梭菌的磷脂酶C(PLC)一起孵育。通过高效液相色谱法(HPLC)和气相色谱法监测发现,PLA(2)导致游离多不饱和脂肪酸显著增加,同时伴有膜磷脂降解。相同浓度的PLC产生的作用远小于PLA(2)。在膜磷脂的脱酰基作用和[(3)H]花生四烯酸掺入方面表现出不同的和有差异的效应。PLA(2)(0.018单位/毫升)使[(3)H]花生四烯酸掺入各种磷脂的量大大减少,而相同浓度的PLC则无效。PLA(2)抑制(Na(+) + K(+))-ATP酶,但对对硝基苯磷酸酶活性无效,而PLC则刺激这两种酶。PLA(2)诱导大脑皮质切片肿胀,而PLC则无效。因此,膜完整性扰动的严重程度以及对脑膜中(Na(+) + K(+))-ATP酶的抑制可能在PLA(2)诱导的大脑切片细胞肿胀中起重要作用。