CELL MEMBRANE MICROVISCOSITY

细胞膜微粘度

基本信息

项目摘要

Change in the microviscosity of cell membranes were shown to modulate the functionality of their receptors, presumably by altering their ability to reorient into more or less active positions. 1) The abnormal accumulation of saturated long chain fatty acids in the inherited disease of adrenoleukodystrophy also result in stiff membranes for when human adrenocortical cells are cultured in their presence, 15 times more ACTH is needed to achieve level of cortisol synthesis. This probably explains the mechanism by which adrenal insufficiency occurs in this disease. 2) Gossypol is a dietary phenolic that has caused outbreaks of infertility in several provinces in china. This compound causes an increase in granulosa cell membrane microviscosity and thereby decreases their estrogen response to FSH. Altered functionality of gonadotropin receptors on target tissues is a likely mechanism by which this phenomenon of infertility occurs. 3) We have shown that the unique 19OH prostaglandins in human semen suppress lymphocytes' response to mitogens 30 times more than PGE2. Preliminary studies demonstrated that they reduce the microviscosity of human lymphocyte membranes, a phenomenon that may be extremely important in explaining the increased susceptability of homosexuals to various infective agents. Other preliminary studies have shown that these same prostaglandins cause a marked decrease in the microviscosity of human membranes, an observation that may be relevant to their role in male reproductive physiology. A direct link between the immune surviellance system and the adrenal gland was established when human monocytes were shown to elaborate a soluble factor that stimulates human adrenocortical cells to synthesize cortisol in vitro. Preliminary studies have indicated that the monocytes and granulocytes of diabetic patients metabolize arachidonic acid in an abnormal fashion. The identity of these metabolites is being established and the possible role in the microvascular disease of diabetes is being studied.
细胞膜微粘度的变化表明 调节其受体的功能,大概是通过 改变他们重新定位到或多或少活跃位置的能力。 1)饱和长链脂肪酸的异常积累 肾上腺脑白质营养不良的遗传性疾病也会导致 培养人肾上腺皮质细胞时使用的硬膜 在他们存在的情况下,需要 15 倍的 ACTH 才能达到水平 皮质醇合成。 这可能解释了该机制 这种疾病发生肾上腺皮质功能减退症。 2) 棉酚是 一种膳食酚类物质,导致了不孕症的爆发 中国的几个省份。 该化合物会导致 颗粒细胞膜微粘度从而降低 他们的雌激素对 FSH 的反应。 改变的功能 靶组织上的促性腺激素受体的可能机制是 从而出现这种不孕现象。 3)我们已经展示了 人类精液中独特的19OH前列腺素抑制 淋巴细胞对有丝分裂原的反应是 PGE2 的 30 倍。 初步研究表明,它们可以减少 人淋巴细胞膜的微粘度现象 这对于解释增加的情况可能极其重要 同性恋者对各种感染因子的易感性。 其他 初步研究表明,这些相同的前列腺素 导致人体微粘度显着降低 膜,这一观察可能与其在 男性生殖生理学。 免疫之间的直接联系 监视系统和肾上腺建立时 人类单核细胞被证明可以制造出一种可溶性因子 刺激人类肾上腺皮质细胞合成皮质醇 体外。 初步研究表明,单核细胞和 糖尿病患者的粒细胞代谢花生四烯酸 一种不正常的时尚。 这些代谢物的身份正在被确定 的建立及其在微血管疾病中的可能作用 糖尿病正在研究中。

项目成果

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