Date of Award


Degree Type


Degree Name

Doctor of Philosophy


The in vivo streptozotocin-induced diabetic rat model of cataract is one of the oldest animal models of cataractogenesis available, however investigation of diabetic lenses before the formation of liquid-filled vacuoles, is lacking. Using analysis specific for glutathione, it was found that pre-vacuolar diabetic rat lenses lost glutathione (GSH) (85%) compared to normal lenses. Glutathione disulphide (GSSG) did not appear in diabetic lenses. Lens ascorbate concentration was also decreased by 48% in pre-vacuolar diabetic lenses compared to normal lenses.;ATP loss, previously demonstrated only in post-vacuolar diabetic lenses, was found in pre-vacuolar diabetic lenses compared to normal lenses. It is possible that GSH and ATP interact in a vicious cycle where the loss of one contributes to the loss of the other because the production of one requires an adequate supply of the other.;Osmotic stress due to sorbitol elevation in the diabetic rat lens may not be fully responsible for cataractogenesis. Lens free-amino acid concentrations were decreased by 85% in pre-vacuolar diabetic rat lenses compared to normal rat lenses. Most of this decrease was due to a loss of the amino acid taurine. Pre-vacuolar diabetic lenses did not display increased hydration, therefore the loss of amino acids and GSH may provide osmotic compensation prior to vacuole formation.;These findings support a fundamental alteration to our view of the in vivo diabetic rat lens model. That is, the above biochemical alterations are actually occurring before the formation of initial vacuoles in the lens, as opposed to becoming altered after the formation of vacuoles.



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