The mechanism of oxidative damage to the lens through intraocular photochemical generation of superoxide and its derivatization to other oxidants such as singlet oxygen, hydroxyl radical and hydrogen peroxide has been studied. Rat lenses when organ cultured aerobically in TC 199 containing additional amounts of riboflavin were damaged as demonstrated by an inhibition of the uptake of Rb 86 against a concentration gradient. The pump was not affected by light if the culture was conducted in the basal TC 199. However, light was observed to induce significant peroxidative degradation of the tissue lipids even in the basal medium, the degradation being indicated by the formation of malonaldehyde. Both the inhibition of the pump as well as the peroxidative degradation of the tissue lipids, were attenuated considerably by scavengers of superoxide and hydrogen peroxide. In addition, the lipid degradation was prevented by vitamins C and E. The results suggest that the photodynamic injury to the lens cation pump as well as to membrane lipids is incumbent upon an initial generation of superoxide and its derivatization to other oxidants. Thus, the ocular lens is susceptible to oxidative insult and physiological damage through photocatalytic generation of various oxygen radicals. Large concentrations of ascorbic acid in the aqueous humor seems to be able to provide significant protection against such an insult. Thus, this may be one of the functions of high concentration of ascorbic acid in the aqueous humor. The implication of oxidative stress has also been examined in the genesis of cataracts in vivo. Treatment with vitamin E of the Emory mouse led to a decrease in the rate of cataract progression suggesting that at least in some instances an oxidative stress could participate in the formation of cataracts. Oxygen radicals may inflict damage at multifarious biochemical sites. Human lens lipids were also shown to have an absorption maxima at 239 nm indicating their susceptibility to oxidative degradation. In addition the lipid extract has fluorescence similar to that of lipofuscins. The levels of MDA were higher in the brunescent cataracts as compared to that in the nonbrunescent cataracts. The implications of oxidative stress towards the genesis of cataracts in humans is being explored further.

The cation pump activity of the ocular lens was damaged by exposure to light in the presence of riboflavin phosphate. The intensit of ight was similar to that used for reading purposes. The observed light-induced damage was due to superoxide or its derivatives, the superoxide being produced photochemically. Such damage was attenuated by vitamin C in amounts comparable to that in the aqueous humor. Thus, a new role for the high ascorbate level present in the anterior chamber fluid and the lens has been suggested. Ascorbate in other tissues also might have this novel physiological function of protecting against damage due to superoxide and its derivatives produced during normal cellular oxidation. The concentration of ascorbic acid (vitamin C) in the aqueous humor of man, monkey, and many other animals is one of the highest among the various body fluids (1). The prevalence of this high level of ascorbate has been attributed to the ability of the ciliary epithelium to transport this compound actively from the plasma to the posterior chamber through the blood aqueous barrier (2). For reasons undefined at the present time, the concentration of ascorbate is also high in tissues surrounding the aqueous humor-namely, the cornea and the lens. The concentration in the latter tissue in many instances is second only to that in adrenals (1). Although the importance of ascorbic acid in hydroxylation reactions is known in many tissues, the relevance of a high ascorbate level in the aqueous humor and the lens is not precisely known, although it has been suggested that photochemical oxidation of ascorbic acid in the anterior chamber serves to provide hydrogen peroxide to the lens. The peroxide, in turn, may regulate the tissue hexose monophosphate shunt through the following series of interlinked reactions

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A Hill-Sachs lesion is best differentiated from the anatomic groove by means of its more cephalic position along the longitudinal humeral axis.

Exposure of mice to hyperbaric oxygen leads to an inhibition of the mitotic activity in the germinative epithelium of the lens. This is followed by an eventual development of cataracts. Cataracts have also been observed in human beings treated with hyperbaric oxygen for different afflictions. The lens damage and cataract formation appears to be due to in situ generation of active radicals and other active species of oxygen. These oxygen derivatives may also contribute to the multifactorial process of senile cataract formation in human beings. This hypothesis is based on in vitro experiments with rat lenses cultured in medium generating oxygen radicals, the generation of the radicals being accomplished either photochemically or enzymatically. The ability of the lens to transport rubidium and amino acids from such a medium is adversely affected. This is a recognized index of the damage to the tissue physiology. Scavengers of active oxygen species have been found to protect against this damage. Ascorbate, present in concentrations similar to that in the primate aqueous and lens, is also protective. The studies, therefore, point to an antioxidant and perhaps an anti cataract effect of ascorbate. Pyruvate is another agent useful in this regard.