Dietary sugar and salt represent etiological risk factors of human cataract. To verify etiological data on the basis of histological findings, 9 pigs with a body weight of 40 kg, 3 months of age, in groups of 3 were continuously fed with 5% of refined dietary sugar (sucrose – C12H22O11), 0.5% of salt (NaCl) and a sugar-salt mixture (2.5 + 0.25% accordingly) in their crude (unboiled) meal food during 3 months, which resulted in minor cataractous changes in the lens. In the second experiment, 10 weight- and age-matched animals were fed a chronic sugar and intermittent salt diet during 6 months; the other 10 animals served as controls. During the second experiment, crystallin leakage into the aqueous humor of the lens was detected, and a marked swelling of the lens fibers and fiber tips was noticed, indicating that excessive amounts of dietary sugar and salt are risk factors for the development of cataract in normal (nondiabetic) animals.
Feeding experimental animals (19 pigs) with surplus sucrose and salt (NaCl) caused cataractous changes in lens tissue and triggered the formation of pseudoexfoliative material on the lens capsule. In the control animals (15 pigs) pseudoexfoliative material was absent. The avidin-biotin complex immunohistochemical method was applied to the pseudoexfoliative material obtained from 15 porcine experimental precataractous lenses and 1 spontaneously cataractous eye and revealed crystallins as a component of the intraocular pseudoexfoliative material. To prevent the development of both intraocular pseudoexfoliative material and crystallin-dependent glaucomatous changes in the trabecular meshwork of the eye, it is important to avoid any cataractogenic insult, including surplus sucrose and salt consumption, causing crystallin leakage from the lens.
Abnormal epithelioid, fibroblast-like, infiltrating, and bladder cell complexes of fetal swine organ-cultured lenses contained DNA-synthesizing cells, of which epithelioid and fibroblast-like cells proliferated. The same is supposed to be true for abnormal cells of human cataractous lenses.
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