Pulido J A, del Hoyo N, Pérez-Albarsanz M A
Departamento de Bioquímica y Biología Molecular, Universidad de Alcalá, Madrid, Spain.
Life Sci. 1992;50(21):1585-96. doi: 10.1016/0024-3205(92)90444-t.
The inositol lipids from rat brain miniprisms were deacylated and separated by anion-exchange chromatography in order to determine whether or not gamma-hexachlorocyclohexane (gamma-HCH, lindane) and related compounds affect the different phosphatidylinositols. The incorporation of myo-[2-3H]inositol into phosphatidylinositol, phosphatidylinositol monophosphate and phosphatidylinositol bisphosphate were inhibited by lindane and its delta-HCH isomer. The inhibitory effects on phosphatidylinositol synthesis are not prominent in alpha-HCH and they are not significant with the beta-HCH and cyclodienes. The results presented here indicate that the inhibitory effect of lindane and delta-HCH on the phosphatidylinositol metabolism was no exclusively due to an interference with glucose transport. Lindane-treated miniprisms showed decreased myo-[2-3H]inositol uptake and, proportionately, an even greater inhibition of inositol phospholipid synthesis. Cellular uptake can, therefore, not account for all of the lindane inhibition.
为了确定γ-六氯环己烷（γ-HCH，林丹）及相关化合物是否会影响不同的磷脂酰肌醇，对大鼠脑微粒体中的肌醇脂质进行了脱酰基处理，并通过阴离子交换色谱法进行分离。林丹及其δ-HCH异构体抑制了肌醇-[2-³H]肌醇掺入磷脂酰肌醇、磷脂酰肌醇单磷酸和磷脂酰肌醇双磷酸的过程。α-HCH对磷脂酰肌醇合成的抑制作用不明显，β-HCH和环二烯则无显著影响。此处呈现的结果表明，林丹和δ-HCH对磷脂酰肌醇代谢的抑制作用并非完全归因于对葡萄糖转运的干扰。经林丹处理的微粒体显示肌醇-[2-³H]肌醇摄取减少，相应地，对肌醇磷脂合成的抑制作用更大。因此，细胞摄取并不能解释林丹的所有抑制作用。
