Previous work has demonstrated that photochemically induced oxidative stress generated with 4 microM
riboflavin in a 4%
oxygen atmosphere utilizing daylight type radiation is capable of causing
cataract in cultured rat
lenses. Such
cataract is prevented by the GSH
peroxidase type mimic,
AL-3823A. Examination of the early stages of
cataract formation produced by short-term oxidative stress and recovery is now reported. A 24-hr oxidative stress, under the above conditions, causes loss of transparency, particularly in the equatorial region, increased hydration, loss of glyceraldehyde-3-PO4
dehydrogenase activity, oxidation of non-
protein thiol and a decrease in 86Rb and [14C]
choline uptake and
ATP levels. Examination of recovery of these parameters during a 72-hr period indicates, in most cases, little or no reversal of oxidative damage. Hydration and loss of non-
protein thiol continued during the recovery period. The presence of
AL-3823A during the stress period prevented change in all parameters. Transport systems appear to be particularly vulnerable to this type of oxidative stress losing 50% or more activity within 4 hr. Even after a 2-hr stress,
choline transport did not recover even though, under these conditions,
ATP levels had only decreased slightly. Cytosolic components such as non-
protein thiol and glyceraldehyde-3-PO4
dehydrogenase also showed little change after a 4-hr insult. 86Rb efflux experiments indicated no change in permeability during a 24-hr stress period. The overall conclusion from these studies is that a 24-hr oxidative stress which appears to reflect physiological conditions existing during
cataract development, causes extensive, irreversible damage.(ABSTRACT TRUNCATED AT 250 WORDS)