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渗透应激对大鼠晶状体中磷酸胆碱流出及周转的影响。

Effect of osmotic stress on phosphorylcholine efflux and turnover in rat lenses.

作者信息

Desouky M A, Geller A M, Jernigan H M

机构信息

Department of Ophthalmology, University of Tennessee, Memphis 38163.

出版信息

Exp Eye Res. 1992 Feb;54(2):269-76. doi: 10.1016/s0014-4835(05)80217-9.

DOI:10.1016/s0014-4835(05)80217-9
PMID:1559554
Abstract

The concentration of the phospholipid precursor, phosphorylcholine (P-choline), is greater than 10 mM in rat lenses. Cataractogenic osmotic or oxidative stress affects lenticular choline uptake and metabolism and decreases the P-choline concentration. To study the mechanism(s) of the decrease in P-choline concentration induced by the cataractogenic sugars, xylose, galactose or glucose, rat lenses were first incubated in TC-199 medium containing [3H]choline, and then the metabolism of the resulting lenticular P-[3H]choline was followed in culture. Lenses which were osmotically stressed by incubation in TC-199 medium with 30 mM xylose lost more than 50% of their P-[3H]choline within 48 hr. Most of the P-[3H]choline lost from the stressed lenses was recovered in the incubation medium as P-[3H]choline, indicating that leakage of P-choline from the osmotically damaged lenses was the principal factor contributing to the decrease. Leakage of P-[3H]choline from lenses in the xylose medium was about three-fold greater than in the control medium, which contained 30 mM fructose. The turnover of the P-choline pool in rat lenses was also studied, and the concentration of P-choline was found to be a balance between hydrolysis and synthesis. The hydrolysis of lenticular P-choline was similar in xylose or control medium. In contrast, P-choline synthesis is slower in osmotically stressed lenses, resulting in a net conversion of P-[3H]choline to [3H]choline in the stressed lenses. Because some of the [3H]choline derived from P-choline hydrolysis was lost to the surrounding culture medium, this mechanism also contributed to the decreased P-choline in lenses incubated with xylose.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在大鼠晶状体中,磷脂前体磷酸胆碱(P - 胆碱)的浓度大于10 mM。致白内障的渗透压或氧化应激会影响晶状体对胆碱的摄取和代谢,并降低P - 胆碱的浓度。为了研究致白内障糖类(木糖、半乳糖或葡萄糖)诱导P - 胆碱浓度降低的机制,首先将大鼠晶状体在含有[³H]胆碱的TC - 199培养基中孵育,然后在培养过程中追踪由此产生的晶状体P - [³H]胆碱的代谢。在含有30 mM木糖的TC - 199培养基中孵育而受到渗透压应激的晶状体,在48小时内失去了超过50%的P - [³H]胆碱。从受应激晶状体中损失的大部分P - [³H]胆碱在孵育培养基中以P - [³H]胆碱的形式回收,这表明渗透压受损晶状体中P - 胆碱的泄漏是导致浓度降低的主要因素。木糖培养基中晶状体P - [³H]胆碱的泄漏比含有30 mM果糖的对照培养基中大约高三倍。还研究了大鼠晶状体中P - 胆碱池的周转率,发现P - 胆碱的浓度是水解和合成之间的平衡。晶状体P - 胆碱在木糖或对照培养基中的水解相似。相比之下,渗透压应激晶状体中的P - 胆碱合成较慢,导致受应激晶状体中P - [³H]胆碱净转化为[³H]胆碱。由于一些源自P - 胆碱水解的[³H]胆碱损失到周围的培养基中,这种机制也导致了与木糖一起孵育的晶状体中P - 胆碱的减少。(摘要截短至250字)

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