CONTROL OF HEXOSE TRANSPORT IN CULTURED RETINOBLASTOMA

晶状体蛋白质“晶状”可能会受到各种类型的 精神错乱。众所周知，青少年糖尿病或各种 各种类型的半乳糖血症会导致白内障。这些的基础是 白内障通常被归因于葡萄糖或 半乳糖通过转运进入晶状体和随后的酶 还原成相应的多元醇通过大量过剩的 糖还原酶。这种情况造成了渗透性 不平衡，因为累积的多元醇似乎不是 有促进的外流，但必须被动地扩散。这个 随之而来的高渗透最终会把水吸进细小的 晶状体有序结晶，从而造成晶状体白内障。 这似乎是青少年白内障的主要因素。什么类型的 将葡萄糖或半乳糖送入细胞内 镜头，如果有的话，它是如何监管的？己糖运输系统在 成纤维细胞或成肌细胞培养，可下调 葡萄糖是常见的观察对象。我们将把这称为降级- 规范交通“路缘”。我们已经研究了运输 抑制各种品系的仓鼠肺成纤维细胞培养。我们 通过使用突变体pgi获得了一个特别清晰的洞察力 突变，因为它缺乏磷酸葡萄糖异构酶。这意味着 葡萄糖-6-P不能转化为果糖-6-P a 对有氧能量的产生至关重要的转化 新陈代谢对于交通抑制是必不可少的。PGI 突变体只对葡萄糖有很强的抑制作用，但对葡萄糖没有影响 甘露糖、氨基葡萄糖或果糖。令人惊讶的是，这一切- 顺式已糖，D-异构体，被证明是最有效的 运输“Curber”；D-丙硫氨酸不活跃。进一步的进展 取决于放射性标记的D-同种异体的可用性。我们的发现 衣霉素(TN)进一步增强葡萄糖或同种异构体- 诱导抑制(与果糖介质相比，运输能力损失85%) 更值得注意的是，自从从Allse转换到 果糖在6小时内恢复一半的运输能力 无论是否存在TN。这将是非常有意义的 有兴趣将晶状体的己糖转运系统与 视网膜母细胞瘤的视网膜准备或培养，关于 介导的葡萄糖-TN抑制作用。几个小时后。随后进行预孵化 由通常的运输测试将会尝试。

The lens protein "crystalline" can be subject to various types of disorders. It is known that juvenile diabetes mellitus or various types of galactosemia bring about cataracts. The basis for these cataracts has often been ascribed to an entrapment of glucose or galactose by transport into the lens and subsequent enzymatic reduction into the corresponding polyols by the huge excess of sugar reductases. This state of affairs creates osmotic imbalance, due to the fact that the accumulating polyols seem not to have a facilitated efflux but have to diffuse out passively. The ensuing hyperosmosis would eventually draw water into the finely ordered crystalline of the lens and thus create a lens cataract. This seems to be the main factor in juvenile cataracts. What type of hexose transport system drives glucose or galactose into the lens and how is it regulated if at all? Hexose transport systems in fibroblast or myoblast cultures which can be downregulated by glucose are commonly observed. We shall call this down- regulation the transport "CURB". We have studied the transport curb in various lines of hamster lung fibroblast cultures. We obtained a particularly clear insight by using a mutant, the PGI mutant, because it lacks phospho-gluco-isomerase. This means that glucose-6-P cannot be converted to fructose-6-P a conversion which critical for the generation of aerobic energy metabolism which is essential for the transport curb. The PGI mutant shows a strong curb only with glucose, but not with mannose, glucosamine nor fructose. Surprisingly enough, the all- cis aldohexose, D-allose, turned out to be the most effective transport "curber"; D-altrose was inactive. Further progress depends on the availability of radiolabelled D-allose. Our finding that tunicamycin (TN) further intensifies the glucose or allose- induced curb (85% loss of transport capacity vs. fructose medium) is noteworthy so much the more since a switch from allose to fructose restores half the transport capacity within 6 hrs regardless of the presence or absence of TN. It would be of great interest to compare the hexose tansport systems of the lens with that of retina preps or cultures from retinablastoma, in regard to the mediated glucose-TN curb. A few hrs. preincubation followed by the usual transport test will be tried.