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)

Male WBN/Kob rats represent a spontaneously diabetic strain with hyperglycemia, cataracts, nephropathy, neurophathy, pancreatic fibrosis and hyperlipemia. Cataracts and retinal changes in WBN/Kob rats were examined by light and electron microscopy to evaluate the ocular complications. Lens opacity was present in the posterior subcapsular and center of the anterior cortex of male 14-month-old WBN/Kob rats. Light and transmission electron microscopy showed swelling and irregularity of lens fibers. Scanning electron microscopy revealed that lens fibers were irregular and had many granules and bulging processes of various sizes on the cortical side of the opacified region. The nuclear side of the opacified region showed spongy changes and complete absence of lens fibers. Electron microscopy showed retinal degeneration in the photoreceptor outer segments of 1-month-old male WBN/Kob rats. Light microscopy showed thin outer segments and outer nuclear layers in 5-month-old rats, and electron microscopy revealed severe degeneration in the outer segments. The retinas of 11-month-old rats were thinner; the outer plexiform layer was very thin; the photoreceptor cell nuclei in the outer nuclear layer had decreased to one layer and were almost in contact with the inner nuclear layer nuclei, while the visual cells had disappeared. Retinal degeneration had progressed even further in 14-month-old rats, and very few photoreceptor cell nuclei remained. The retinal capillary lumens were small, and their pericytes had thickened basement membranes. The basement membranes of retinal capillaries from WBN/Kob rats were significantly thicker than those from control Wistar rats (p < 0.0001). Although this rat has spontaneous diabetic features, such as cataracts, its retinal changes look more degenerative.
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PMID:Lens and retinal changes in the WBN/Kob rat (spontaneously diabetic strain). Electron-microscopic study. 966 53

Melatonin (N-acetyl-5-methoxytryptamine) is an indoleamine with a range of antioxidative properties. Melatonin is endogenously produced in the eye and in other organs. Current evidence suggests that melatonin may act as a protective agent in ocular conditions such as photo-keratitis, cataract, glaucoma, retinopathy of prematurity and ischemia/reperfusion injury. These diseases are sight-threatening and they currently remain, for the most part, untreatable. The pathogenesis of these conditions is not entirely clear but oxidative stress has been proposed as one of the causative factors. Elevated levels of various reactive oxygen and nitrogen species have been identified in diseased ocular structures. These reactants damage the structure and deplete the eye of natural defense systems, such as the antioxidant, reduced glutathione, and the antioxidant enzyme superoxide dismutase. Oxidative damage in the eye leads to apoptotic degeneration of retinal neurons and fluid accumulation. Retinal degeneration decreases visual sensitivity and even a small change in the fluid content of the cornea and crystalline lens is sufficient to disrupt ocular transparency. In the eye, melatonin is produced in the retina and in the ciliary body. Continuous regeneration of melatonin in the eye offers a frontier antioxidative defense for both the anterior and posterior eye. However, melatonin production is minimal in newborns and its production gradually wanes in aging individuals as indicated by the large drop in circulating blood concentrations of the indoleamine. These individuals are possibly at risk of contracting degenerative eye diseases that are free radical-based. Supplementation with melatonin, a potent antioxidant, in especially the aged population should be considered as a prophylaxis to preserve visual functions. It may benefit many individuals worldwide, especially in countries where access to medical facilities is limited.
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PMID:Protective effects of melatonin in experimental free radical-related ocular diseases. 1644 46

The ubiquitin-proteasome pathway (UPP) plays important roles in many cellular functions, such as protein quality control, cell cycle control, and signal transduction. The selective degradation of aberrant proteins by the UPP is essential for the timely removal of potential cytotoxic damaged or otherwise abnormal proteins. Conversely, accumulation of the cytotoxic abnormal proteins in eye tissues is etiologically associated with many age-related eye diseases such as retina degeneration, cataract, and certain types of glaucoma. Age- or stress-induced impairment or overburdening of the UPP appears to contribute to the accumulation of abnormal proteins in eye tissues. Cell cycle and signal transduction are regulated by the conditional UPP-dependent degradation of the regulators of these processes. Impairment or overburdening of the UPP could also result in dysregulation of cell cycle control and signal transduction. The consequences of the improper cell cycle and signal transduction include defects in ocular development, wound healing, angiogenesis, or inflammatory responses. Methods that enhance or preserve UPP function or reduce its burden may be useful strategies for preventing age-related eye diseases.
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PMID:Role of the ubiquitin-proteasome in protein quality control and signaling: implication in the pathogenesis of eye diseases. 2272 27