Lens cells can synthesize, degrade, and remodel
lipids. Endogenous
lipid synthesis, in conjunction with uptake of exogenous
cholesterol and certain
fatty acids, leads to the formation of a plasma membrane that is especially rich in
sphingomyelin,
cholesterol, and long-chain
saturated fatty acids. As a result of this unusual
lipid composition, lens membranes have very low fluidity, which is restricted even further by
lipid-
protein interactions. The composition and metabolism of
membrane lipids may affect the formation of various types of
cataracts. Diets rich in
vegetable oils offer some protection against the formation of osmotic
cataracts and the hereditary
cataract of the RCS rat, although the mechanism of this effect is not clear.
Vitamin E also protects against the formation of several types of
cataract in vivo and in vitro, suggesting that lipid peroxidation may play a role in cataractogenesis. Certain drugs which inhibit
lipid synthesis or degradation are cataractogenic, and a deficiency in cataractogenic, and a deficiency in
phosphatidylserine is associated with a loss of Na+/K+
ATPase activity in several types of
cataract. Human senile
cataracts show a marked loss of
protein-
lipid interactions, although the overall
lipid composition is normal. This loss of
protein-
lipid interactions may be related to oxidative damage to
membrane-associated proteins. Interestingly, the decrease in the fluidity of lens membranes with age would counteract the formation of aqueous pores in the membrane, which can result from the oxidative cross-linking of
membrane-associated proteins. Certain pathways of lipid metabolism seem to have regulatory functions. Among these are
phosphatidylinositol turnover,
phosphatidylethanolamine methylation, and
arachidonic acid metabolism. All of these pathways function in the lens.
Phosphatidylinositol turnover is correlated with the rate of lens epithelial cell division, while
phosphatidylethanolamine methylation seems to be related to the initiation of lens fiber cell formation. Both pathways are associated with the release and metabolism of
arachidonic acid in other cell types. While it is not known whether
phosphatidylinositol turnover or
phosphatidylethanolamine methylation result in the release of
arachidonic acid in the lens, recent work has shown that lens cells from a variety of species can metabolize
arachidonic acid by both the
cyclooxygenase and
lipoxygenase pathways. The possible physiological significance of these metabolites to the lens is yet to be determined.