Cholesterol oxidation reduces Ca(2+)+MG (2+)-ATPase activity, interdigitation, and increases fluidity of brain synaptic plasma membranes.
Cholesterol oxidation reduces Ca(2+)+MG (2+)-ATPase activity, interdigitation, and increases fluidity of brain synaptic plasma membranes.
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胆固醇氧化可降低 Ca(2 ) MG (2 )-ATPase 活性、交叉，并增加脑突触质膜的流动性。
DOI：
10.1016/0006-8993(95)00347-s
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发表时间：
1995
期刊：
影响因子：
2.9
通讯作者：
Avdulov,NA
中科院分区：
文献类型：
--
作者：
Wood,WG;Igbavboa,U;Rao,AM;Schroeder,F;Avdulov,NA
这些实验研究了胆固醇氧化对脑突触质膜（SPM）的Ca ~（2+）+Mg ~（2+）-ATP酶活性、Na ~++K ~+-ATP酶活性和膜结构的影响。胆固醇氧化酶[E.C.1.1.3.6，来自短杆菌属]用来氧化胆固醇两个胆固醇池被确定在突触体膜的基础上，他们的可及性胆固醇氧化酶。胆固醇快速氧化池a1 t12为1.19± 0.09min，第二池a2 t12为38.30± 4.16min。低水平胆固醇氧化可抑制Ca 2 ++ Mg 2 +-ATP酶活性。例如，10%的胆固醇氧化导致约35%的Ca 2 ++ Mg 2 +-ATP酶活性抑制。胆固醇氧化13%后，未观察到Ca ~（2+）+Mg ~（2+）-ATP酶活性的进一步抑制。Na++K+-ATP酶活性不受胆固醇氧化水平（5%-40%）的影响。胆固醇氧化显著减少SPM交错，显著增加流动性。观察到的SPM交错和Ca 2 ++ Mg 2 +-ATP酶活性之间的关系与使用模型膜的研究一致[7]。脑SPM的功能和结构被相对较低水平的胆固醇氧化所改变，这是了解胆固醇动力学和神经元功能的一种新方法。脑SPM对胆固醇氧化的敏感性可能是重要的，相对于氧自由基和某些神经退行性疾病之间的拟议关联。
These experiments examined effects of cholesterol oxidation on Ca2++Mg2+-ATPase activity, Na++K+-ATPase activity, and membrane structure of brain synaptic plasma membranes (SPM). Cholesterol oxidase [E.C.1.1.3.6 from Brevibacterium sp.] was used to oxidize cholesterol. Two cholesterol pools were identified in synaptosomal membranes based on their accessibility to cholesterol oxidase. A rapidly oxidized cholesterol pool was observed with a1t1 2of 1.19±0.09 min and a second pool with a2t1 2of 38.30±4.16 min. Activity of Ca2++Mg2+-ATPase was inhibited by low levels of cholesterol oxidation. Ten percent cholesterol oxidation, for example, resulted in approximately 35% percent inhibition of Ca2++Mg2+-ATPase activity. After 13% cholesterol oxidation, further inhibition of Ca2++Mg2+-ATPase activity was not observed. Activity of Na++K+-ATPase was not affected by different levels of cholesterol oxidation (5%–40%). SPM interdigitation was significantly reduced and fluidity was significantly increased by cholesterol oxidation. The relatiobship observed between SPM interdigitation and Ca2++Mg2+-ATPase activity was consistent with studies using model membranes [7]. Brain SPM function and structure were altered by relatively low levels of cholesterol oxidation and is a new approach to understanding cholesterol dynamics and neuronal function. The sensitivity of brain SPM to cholesterol oxidation may be important with respect to the proposed association between oxygen free radicals and certain neurodegenerative diseases.