Malone J I, Lowitt S, Cook W R
Department of Pediatrics and Diabetes Center, University of South Florida, College of Medicine, Tampa 33612.
Pediatr Res. 1990 Mar;27(3):293-6. doi: 10.1203/00006450-199003000-00019.
It has been suggested that sugar cataracts associated with diabetes mellitus result from the accumulation of excess sorbitol within lens fibrils. Swelling of lens fibrils occurs when water moves in to maintain osmotic balance; the excess water causes disruption of fibrils and cataract formation. Other studies have indicated that more than sorbitol-induced osmotic stress is involved. Our study used lenses collected from rats after 21 or 44 d of streptozotocin diabetes. Cataracts formed in untreated 44-d streptozotocin diabetic rats, but were not apparent in the 21-d untreated diabetic animals. Lens sorbitol increased in the diabetic animals both before and after cataract formation. Lens taurine varied inversely with the sorbitol content in a fashion that resulted in no net change in total lens osmoles. Lens water did not increase in the diabetic animals with or without cataracts. The aldose reductase inhibitor Sorbinil prevented the increase in lens sorbitol in both the 21- and 44-d streptozotocin diabetic rats; cataract formation was prevented in the 44-d diabetic animals. The lens water in untreated diabetic animals with cataracts did not differ from lens water in the Sorbinil-treated diabetic animals that did not develop cataracts. Sorbinil treatment of diabetic animals was associated with normalization of both lens sorbitol and taurine levels. Taurine has been shown to serve both as an osmoregulator and as an antioxidant. The apparent increase in lens osmolality attributed to sorbitol was counterbalanced by an equimolar reduction in taurine concentration. The reciprocal relationship between taurine and sorbitol reduces the likelihood of an osmotic mechanism for sugar cataractogenesis; the reduced lens taurine, however, may increase the risk of lens protein oxidation and subsequent cataract formation. Thus in vivo sugar cataract formation may be an oxidative process rather than an osmotic phenomenon.
有人提出，与糖尿病相关的糖性白内障是由于晶状体纤维内过量山梨醇的积累所致。当水进入以维持渗透平衡时，晶状体纤维就会肿胀；过多的水分会导致纤维破坏和白内障形成。其他研究表明，涉及的不仅仅是山梨醇诱导的渗透应激。我们的研究使用了从链脲佐菌素诱导的糖尿病大鼠21天或44天后收集的晶状体。未治疗的44天链脲佐菌素糖尿病大鼠形成了白内障，但在21天未治疗的糖尿病动物中不明显。糖尿病动物在白内障形成前后晶状体山梨醇均增加。晶状体牛磺酸与山梨醇含量呈反比变化，导致晶状体总渗透压无净变化。有或没有白内障的糖尿病动物晶状体水分均未增加。醛糖还原酶抑制剂索比尼尔可防止21天和44天链脲佐菌素糖尿病大鼠晶状体山梨醇增加；44天糖尿病动物的白内障形成得到预防。有白内障的未治疗糖尿病动物的晶状体水分与未发生白内障的索比尼尔治疗糖尿病动物的晶状体水分没有差异。索比尼尔治疗糖尿病动物与晶状体山梨醇和牛磺酸水平的正常化有关。牛磺酸已被证明既作为渗透压调节剂又作为抗氧化剂。山梨醇导致的晶状体渗透压明显升高被牛磺酸浓度等摩尔降低所抵消。牛磺酸和山梨醇之间的相互关系降低了糖性白内障发生渗透机制的可能性；然而，晶状体牛磺酸减少可能会增加晶状体蛋白质氧化和随后白内障形成的风险。因此，体内糖性白内障形成可能是一个氧化过程而非渗透现象。
