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)

The development of naphthalene cataract in rabbits is described, photographed in detail, and compared with different types of senile cataract in man. The naphthalene cataract can serve as a model for subcapsular senile cataract in man, but not for others.
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PMID:Is the experimental naphthalene cataract a model for human senile cataract? 340 53

When naphthalene was administered at a daily dose of 1 g/kg body weight to Wistar strain rats, their serum lipid peroxide levels were increased on the 4th day after the first administration and reached a maximum on the 7th day. This seems to be due to lipid peroxidation in the liver, in which lipid peroxide levels were increased in a similar pattern as those in the serum. The content of reduced glutathione in lenses of naphthalene-administered rats decreased on the 4th day. These results suggest that in naphthalene-induced cataract in albino rats increased lipid peroxides in the bloodstream may play a role in cataractogenesis.
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PMID:Serum lipid peroxide levels of albino rats administered naphthalene. 375 1

During the last 10-15 years, investigations into the biology and biochemistry of the lens have demonstrated that the age changes observed cannot be the only cause of the formation of senile cataract. The various types of opacities and the wide age range in which they begin indicate a multifactorial origin involving endogenous and exogenous risk factors. Initial epidemiological studies have identified certain risk factors. Experimental cataract research is able to elucidate possible damaging mechanisms by using cataract models, for instance, the cataracts caused by excess carbohydrate (galactose, glucose), naphthalene application, ionizing rays, or by additional cocataractogenics, thus indicating steps for countermeasures. Taking (true) diabetic cataract of rats after Streptozotocin injection as an example, the efficacy of aldose reductase inhibitors is shown. Even if additional cataractogenic factors such as naphthalene and X-rays are applied, diabetic lens opacities can be prevented completely. Damage by naphthalene is due to an increased oxidative change in the lens protein. Several substances promoting the antioxidative capacity of the lens, thereby inhibiting cataract formation, are already available. Preclinical or clinical studies have demonstrated the efficacy of only a few of the commercially available anticataract drugs. The results of animal experiments presented here may well represent a basis for the development of really effective anticataract drugs.
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PMID:[What possibilities exist to modify cataract development on the basis of current biochemical knowledge? Where can drugs act?]. 404 54

Oxidation of tyrosine in the presence of bovine lens proteins leads to the formation of brown or black melanoproteins. Both tyrosinase and the oxidizing system of ferrous sulphate-ascorbic acid-EDTA are effective. The fluorescence of the lens proteins is both altered and enhanced by the tyrosine-oxidizing systems. Their fluorescence spectra resemble those of urea-insoluble proteins of human cataractous lens and of 1,2-naphthaquinone-proteins of naphthalene cataract. The lens proteins lose their thiol groups and, in acid hydrolysates of treated beta-and gamma-crystallins, a substance has been detected chromatographically that behaves similarly to a compound formed when 3,4-dihydroxyphenylalanine (dopa) is oxidized by tyrosinase in the presence of cysteine. Analysis and behaviour of this substance from hydrolysates of lens proteins suggest that it is a compound of cysteine and dopa.
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PMID:Reaction of tyrosine oxidation products with proteins of the lens. 497 Dec 87

1. Cataracts were developed by incubating rabbit lenses for 22hr. at 37 degrees in a culture medium containing tyrosine and tyrosinase (EC 1.10.3.1). 2. A 45% diminution in the content of GSH and significant inhibition of glucose 6-phosphate dehydrogenase (EC 1.1.1.49) activity were observed in the cataractous lenses compared with controls. 3. GSSG accumulated in both cataractous and control lenses. Significant amounts of GSSG were transported outward from the cataractous lenses and small amounts from control lenses. 4. Transport of GSSG from rabbit lens incubated in a diffusate of plasma from a naphthalene-fed rabbit was also observed. 5. GSSG was found in the aqueous humour obtained between 2 and 24hr. after feeding of naphthalene to rabbits; subsequently the GSSG in the aqueous humour decreased to almost undetectable amounts in 48hr.; in controls, GSSG was not detectable. 6. A possible mechanism of formation of experimental and senile cataract is briefly discussed.
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PMID:Cataract produced by tyrosinase and tyrosine systems in rabbitens in vitro. 497 83

Development of experimental cataract can be objectively monitored in rats by application of Scheimpflug photography with the SL 45 Topcon camera and subsequent densitometric image analysis. The method has been used to study naphthalene cataract in Brown-Norway rats (BN-CPB), as well as diabetic cataract induced by streptozotocin injection in Sprague-Dawley rats. The values obtained by linear microdensitometric image analysis allowed precise characterization of the opacification with respect to size, topography, and time progress so that statistical evaluation of the efficacy of certain drugs in prevention or delay of experimental cataracts was possible.
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PMID:Long-term follow-up examination of experimental cataracts in rats by Scheimpflug photography and densitometry. 651 Jul 20

The tissue localization and subcellular distribution of drug-metabolizing enzymes in the eye are described. With the use of inbred strains of mice, the [Ah] complex is shown to be an important experimental system for probing genetic differences in drug metabolism and related drug toxicities. Although the genetic system described in detail here involves mice, there is ample evidence that the same system operates in man. Genetic differences in acetaminophen- and naphthalene-induced cataract formation and and other ocular degeneration are shown to be related to the [Ah] complex. Because this toxicity appears similar to senile cataracts, we propose that certain types of drug-induced cataracts might exist among clinical populations of senile cataracts but that any cause-and-effect relationship would be very difficult to determine because of underlying interindividual differences in genetic predisposition. It is therefore suggested that genetic differences in drug metabolism be an important consideration in the clinical assessment of ocular toxicity caused by drugs and other environmental pollutants.
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PMID:Genetic differences in drug metabolism associated with ocular toxicity. 704 72

The excised rat crystalline lens opacified when incubated aerobically with phenazine methosulfate, but no opacification was observed under anaerobic conditions. Morphological studies revealed development of opacification in the cortex. The opacification resembled that often seen in the early period of senile cataract as well as in naphthalene-induced and UV cataract. Both an increase in hydration and in electrolyte imbalance accompanied this opacification. Na,K-ATPase activity of the opacified lens was found to decrease. In order to investigate if activated oxygen is involved in these processes, we conducted an electron spin resonance study by means of a spin trapping technique. When the lens homogate was incubated with phenazine methosulfate, OH radicals were generated under aerobic but not under anaerobic conditions. Reduced pyridine nucleotides must be involved in the process, because the mixture of nicotinamide adenine dinucleotide phosphate [NAD(P)] and phenazine methosulfate did not generate OH radicals, but the mixture of NAD(P)H and phenazine methosulfate generates OH radicals, indicating that reduced phenazine methosulfate was involved in the OH radical generation. Probably, the generated OH radicals inactivated Na,K-ATPase residing in the epithelium of the lens, which eventually caused opacification of the lens. The present experiment system may be used for the elucidation of lens opacification (cataract) involved with reactive oxygen species.
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PMID:Reactive oxygen species involved in phenazine-methosulfate-induced rat lens opacification. An experimental model of cataract. 813 88

The progression of naphthalene cataracts induced in Brown-Norway rats and Sprague-Dawley rats was compared. The quality of lens changes was basically the same in both strains. However, the cataract progression in Brown-Norway rats showed regularity and was fast as compared with the progression in Sprague-Dawley rats. The cataract development could be divided into three stages. Stage 1: formation of water clefts below the anterior lens capsule (shallow cortex) was observed as the initial change; stage 2: these water clefts extended into the deeper cortical layers, and a semicircular opaque band at the deeper cortical region becomes visible; stage 3: a retroillumination image revealed a ring shadow formation - slit image observation showed wedge-shaped cortical and deeper cortical zonular opacification as the final stage. The expression of these three stages in Sprague-Dawley rats is less uniform and timely delayed as compared with Brown-Norway rats.
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PMID:Differences in naphthalene cataract formation between albino and pigmented rat eyes. 844 64

Porcine and bovine lens GSTs were compared in the stability against various oxidative stress which is a major factor of cataract formation in order to clarify the role of lens glutathione S-transferase (GST) and its relation to cataractogenesis. Class pi porcine lens GST was inactivated reversibly by biological disulfides, cystine and cystamine, and also inactivated by active oxygen species such as O2- generated through xanthine-xanthine oxidase system and H2O2. On the other hand, class mu bovine lens GST was insensitive to such applied oxidative stress. Furthermore, 1,2-naphthoquinone, which is a metabolite of naphthalene and an actual inducer of naphthalene cataract, strongly inactivated porcine lens GST though it did not affect bovine enzyme. Thus, porcine and bovine lens GSTs had different sensitivity to various oxidative stress which could induce cataract formation. The results suggest that the differential expression of GST isozymes among animals may explain the variation in the cataract formation caused by oxidative stress.
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PMID:Difference in glutathione S-transferase response to oxidative stress between porcine and bovine lens. 847 85


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