Decreased ascorbic acid entry into cornea of streptozotocin-diabetic rats and guinea-pigs

High L-ascorbic acid (AA) levels in aqueous humor and intraocular tissues including lens and cornea are thought to protect against the harmful effects of the photochemical and ambient oxidation reactions involving oxygen and its radicals. Our pulse-chase studies follow a bolus of radiolabeled test molecules including [14C]L-ascorbic acid and [3H]L-glucose (L-glu) introduced into the blood at time t = 0, and determine the time-dependent concentrations of these labeled molecules as they move into aqueous humor, corneal endothelium and stroma tissues. Calculated entry and exit rate constants provide a representative measure of the functional state of passive and carrier mediated transport mechanisms in situ in normal and diabetic animals. Diabetic rats were categorized in terms of length of time exposed to a uniform, monitored streptozotocin (stz) diabetes as: short term (10-20 days); mid-term (40-60 days); and long term (100+ days). In the rat, we observed little change in entry rate of L-glu (a passive marker) into aqueous humor [control Ki = 0.0216 +/- 0.0021 (n = 14)/mid-term stz-diabetes Ki = 0.0202 +/- 0.0027 (n = 10)] and a modest decrease in the entry rate of AA into aqueous humor [control KAi = 0.0231 +/- 0.0022 (n = 14)/mid-term stz-diabetes KAi = 0.0201 +/- 0.0034 (n = 10)]. At corneal endothelium, we noted a significant decrease in the active movement of AA [control KE = 0.614 +/- 0.053 (n = 14)/mid-term stz-diabetes KE = 0.220 +/- 0.026 (n = 9)] while the passive L-glu entry rate remained essentially unchanged.+