Activation of rat brain protein kinase C by lipid oxidation products.
Activation of rat brain protein kinase C by lipid oxidation products.
复制标题
脂质氧化产物激活大鼠脑蛋白激酶 C。
DOI：
10.1016/s0006-291x(88)81293-2
复制
发表时间：
1988
影响因子：
3.1
通讯作者：
Marnett,LJ
中科院分区：
文献类型：
--
作者：
O'Brian,CA;Ward,NE;Weinstein,IB;Bull,AW;Marnett,LJ
膜脂中的不饱和脂肪酸组分在体外和体内都易氧化。最初的氧化产物是过氧化氢脂肪酸，它们自发或酶促转化为多种产物。油酸、亚油酸或花生四烯酸的过氧化氢衍生物刺激从大鼠脑中纯化的蛋白激酶C（PKC）的活性。氢过氧酸满足PKC对磷脂的要求（例如，磷脂酰丝氨酸）。在存在或不存在ImM Ca2+的情况下观察到活化。将氢过氧化物还原成醇或将氢过氧化物脱水成酮可使Kafor活化增加三至四倍，但不会显著降低PKC活化的最大程度。通过氢过氧酸活化的Ka约为未氧化脂肪酸所表现出的值的一半。由于不饱和脂肪酸氧化为氢过氧化物是脂质过氧化反应的第一个事件，因此氢过氧脂肪酸激活PKC可能是细胞对氧化应激的早期反应。
The unsaturated fatty acid components of membrane lipids are susceptible to oxidationin vitroandin vivo. The initial oxidation products are hydroperoxy fatty acids that are converted spontaneously or enzymatically to a variety of products. Hydroperoxy derivatives of oleic, linoleic, or arachidonic acids stimulate the activity of protein kinase C (PKC) purified from rat brain. The hydroperoxy acids satisfy the requirement of PKC for phospholipid (e.g., phosphatidylserine). Activation is observed in the presence or absence of 1 mM Ca2+. Reduction of the hydroperoxides to alcohols or dehydration of the hydroperoxides to ketones increases the Kafor activation three- to fourfold but does not significantly reduce the maximal extent of PKC activation. The Ka's for activation by hydroperoxy acids are approximately half the values exhibited by the unoxidized fatty acids. Since oxidation of unsaturated fatty acids to hydroperoxides is the first event in lipid peroxidation, activation of PKC by hydroperoxy fatty acids may be an early cellular response to oxidative stress.