Modeling Cortical Cataractogenesis: IX Activity of Vitamin E and Esters in Preventing Cataracts and γ‐Crystallin Leakage from Lenses in Diabetic Rats

Abstract

Normal and streptozotocin diabetic female Wistar rats were given vitamin E in the diet as the tocopherol, acetate, or succinate form (2,850 IU/kg food). At the end of 6 weeks, the rats were examined for weight gain or loss, general body condition, and cataracts. At sacrifice, blood was collected for measurement of serum glucose, and gamma-crystallin levels were measured in aqueous and vitreous humors using a radioimmunoassay. One lens was homogenized in 8 M guanidinium chloride for ATP analysis. In normal rats, gamma-crystallin was detected in both aqueous and vitreous humors, with the higher concentration in the vitreous humor. Diabetes caused a sixfold increase in gamma-crystallin in both the aqueous and vitreous humors. Diabetes also led to a significant worsening in general body condition, loss of body weight, formation of cataracts, and decrease in lens ATP levels. Addition of vitamin E and vitamin E succinate, but not vitamin E acetate, to the diet resulted in reduction of gamma-crystallin leakage into the vitreous humors and an increase in body weight. There was no improvement noted for the lens ATP levels, the general body condition, or visual cataract score. Neither streptozotocin-induced diabetes nor vitamin E in the diet appeared to affect the weight of the lenses.

Modelling Cortical Cataractogenesis 21: In Diabetic Rat Lenses Taurine Supplementation Partially Reduces Damage Resulting from Osmotic Compensation Leading to Osmolyte Loss and Antioxidant Depletion

“…Unfortunately their work did not describe the appearance of the lenses, so for the short term experiments it is not specifically known that the lenses were clear, as is the case at 1 and 2 weeks in the diabetic rat. The loss of ATP was previously shown to occur in all sugar cataracts even though the lens remained clear when treated with antioxidants such as BHT (Linklater et al, 1986), vitamin E (Trevithick et al, 1989), vitamin C (Linklater et al, 1990) and vitamin A (Linklater et al, 1992). A possible explanation of this was noted by , who observed that early in the precataractous stages of model diabetic cataract loss of mitochondria occurred.…”

Diabetes-induced changes in lens antioxidant status, glucose utilization and energy metabolism: effect of DL-?-lipoic acid

“…The importance of oxidative stress in various types of experimentally induced cataractogenesis is well established [10] but its role in diabetes-induced cataractogenesis remains a subject of debate. Some reports indicate an important role for oxidative damage in the onset and progression of diabetic cataracts [11], but others failed to demonstrate any substantial retardation of post-translational modification of lens crystallins [12] or cataract formation [13] with antioxidant therapy. At the same time, numerous studies in models of diabetes and galactosaemia suggest that the loss of major antioxidants such as reduced glutathione (GSH), taurine, and ascorbate is a result of osmotic compensation [14±16].…”

Superoxide Dismutase, Catalase, Glutathione Peroxidase and Xanthine Oxidase in Diabetic Rat Lenses

“…In addition, there are several nonenzymatic free radical scavengers, such as glutathione [11], ascorbate [12] and vitamin E [13]. Some metabolic events may lead to alterations in the activities of these enzymes leading to an increase in free radical production.…”