Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Most of the research on AA metabolites in the eye has been concerned with the role of prostaglandins in ocular inflammations. For example, it has been postulated that cystoid macular edema (CME) is due to accumulation of prostaglandins produced after cataract surgery and that indomethacin prevents the development of CME (Tennant, 1976; Milch and Yannuzzi, 1987). It is not known if the retina is the source of these prostaglandins. Cyclooxygenase and lipoxygenase activities have been demonstrated in the retina. In this chapter, evidence is presented indicating that eicosanoids can also be involved in retinal neurotransmission and cell to cell interaction. The mammalian retina contains a relatively large amount of AA esterified to membrane phospholipids. A release of AA takes place in the retina under various experimental conditions, e.g., anoxia, K+ polarization, and light exposure. This release of AA, a prerequisite for eicosanoid syntheses, is produced by phospholipases and lipases, some of which are regulated by receptor-mediated G-proteins. Prostaglandins can act as modulators of postsynaptic responses; some can also alter the electroretinographic response, for example PGD2 selectively increases during light stimulation. An increase in LTC4 occurs in the neural retina after Ca+ ionophore stimulation and an increase in LTC4 released from retinal pigment epithelium occurs after light onset before massive shedding, suggesting an involvement of 5-lipoxygenase metabolites in the initial steps of ROS phagocytosis. Although great advances have been made regarding the function of eicosanoids in the central nervous system (of which the retina is a constitutive part), it is yet a very difficult task to determine to what extent eicosanoids are involved in the action of neurotransmitters and whether they may act as neuromodulators. This is due to the complexity of the synaptic circuitry of the retina, which makes it difficult to define their sources and physiological significance.
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PMID:Metabolism of arachidonic acid in the retina and retinal pigment epithelium: biological effects of oxygenated metabolites of arachidonic acid. 250 22

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.
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PMID:Lens lipids. 639 28

has been described in humans and many animal species. Traumatic rupture of the lens capsule may result in vision-threatening intraocular inflammation that is poorly responsive to medical management. Phthisis bulbi, persistent uveitis or glaucoma often occurs in these eyes. Surgical removal of the lens material is generally indicated shortly after the injury in an effort to preserve vision. Leaking of lens proteins through an intact lens capsule may result in a lympho-plasmacytic anterior uveitis. This is most commonly associated with the presence of a hypermature cataract. The presence of lens-induced uveitis prior to cataract surgery significantly reduces the success rate of cataract surgery. Small amounts of circulating lens proteins maintain a normal T-cell tolerance for lens proteins. Lens-induced uveitis develops when a breakdown occurs of this normal T-cell tolerance. Immune complexes play an important role in the tissue damage associated with the ensuing inflammation. Other factors associated with the tissue damage include hydroxyl radicals, nitroxide radicals, and hydrogen peroxide and arachidonic acid metabolites. Treatment consists of topical and systemic anti-inflammatory medications, mydriatic agents, and glaucoma medications when indicated. Experimental pharmacological agents include dual cyclooxygenase/lipoxygenase inhibitors, interleukin-1 blockers, antioxidants and hydroxyl radical scavengers.
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PMID:Lens-induced uveitis. 1139 8