Klimov A N, Nikiforova A A, Pleskov V M, Kuz'min A A, Kalashnikova N N
Biokhimiia. 1989 Jan;54(1):118-23.
The role of high density lipoproteins (HDL), their subfractions (HDL2 and HDL3) and lecithin: cholesterol acyltransferase (LCAT) on peroxidative modification of low density lipoproteins (LDL) in vitro was studied. Peroxidative modification was estimated by the formation of malonic dialdehyde (MDA) and LDL aggregates during LDL incubation at 37 degrees C for several days without Fe2+ or for 2 hours in the presence of Fe2+ in EDTA-free media. It was shown that the addition of HDL3 (but not HDL2) markedly decreases the formation of both MDA and LDL aggregates. Since LCAT is bound to HDL3, its effect was examined. An addition of LCAT isolated from human plasma (650-fold purification) at a concentration of 450 micrograms/ml resulted in a complete inhibition of LDL peroxidation and LDL aggregate formation. Heat-inactivated LCAT had no effect. Possible mechanisms of the protective effect of LCAT on LDL peroxidative modification are discussed.
研究了高密度脂蛋白(HDL)及其亚组分(HDL2和HDL3)以及卵磷脂胆固醇酰基转移酶(LCAT)在体外对低密度脂蛋白(LDL)过氧化修饰的作用。在无Fe2+的情况下,将LDL于37℃孵育数天,或在无EDTA培养基中存在Fe2+的情况下孵育2小时,通过丙二醛(MDA)的形成和LDL聚集体来评估过氧化修饰。结果表明,添加HDL3(而非HDL2)可显著减少MDA和LDL聚集体的形成。由于LCAT与HDL3结合,因此对其作用进行了研究。添加从人血浆中分离的LCAT(650倍纯化),浓度为450微克/毫升,可完全抑制LDL过氧化和LDL聚集体的形成。热灭活的LCAT无此作用。讨论了LCAT对LDL过氧化修饰保护作用的可能机制。