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)

A total of 125 human lenses (97 senile cataractous and 28 clear) were analyzed by means of neutron activation analysis for trace element concentrations of copper, zinc, manganese, cobalt, rubidium, scandium, and nickel. Tt was found that the rubidium concentration remarkably decreased and the copper concentration moderately increased with the progression of cataract. The concentrations of manganese, zinc, and cobalt showed some fluctuations without a definite increase or decrease, and the scandium and nickel content was found to be very low.
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PMID:Investigations on trace elements in normal and senile cataractous lenses. Activation analysis of copper, zinc, manganese, cobalt, rubidium, scandium, and nickel. 30 83

Intact rat lenses were incubated in riboflavin-containing Tyrode solution or medium-199, generating photochemically active species of oxygen and the oxidative stress measured in terms of the decrease in active accumulation of rubidium, and the fall in the levels of glutathione and ATP. Addition of pyruvate to the medium prevented the tissue against oxidative damage as evidenced by a greater accumulation of rubidium and higher levels of glutathione and ATP. Pyruvate was thus found to be effective against the toxicity of oxygen derivatives, particularly the hydrogen peroxide. In dark experiments also, conducted in glucose-free medium, the uptake of rubidium was substantially greater in the presence of pyruvate. The levels of ATP were also higher. These results, therefore, suggest that this ketoacid is beneficial to the tissue through its ability to decompose H2O2 as well through providing a metabolic support. The development of in vitro cataract under the photochemical effects of riboflavin and oxygen was also effectively thwarted by pyruvate. The results are thus potentially useful from the point of view of developing pyruvate and similar compounds as effective anticataract agents.
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PMID:Photoinduction of cataracts in rat lens in vitro. Preventive effect of pyruvate. 237 72

When rat lens is incubated in 30 mM galactose overnight, the extent of accumulation of rubidium ions (Rb) and myoinositol (MI) are affected, as well as the Na-K ATPase activity. Rb accumulation and Na-K ATPase activity are only slightly affected compared to the dramatic drop in MI accumulation. These changes are completely abolished by sorbinil, which blocks polyol formation, or by rendering the galactose medium hypertonic to offset the osmotic effect of polyol formation. On the other hand, the addition of excess MI to the galactose medium had no effect on correcting these changes. The results obtained are consistent with the polyol-osmotic theory of sugar cataract formation.
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PMID:The accumulation of myoinositol and rubidium ions in galactose-exposed rat lens. 301 19

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.
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PMID:Ascorbic acid and the eye lens. 318 90

Intact rat lenses incubated with lumazine and xanthine oxidase are physiologically damaged as evidenced by a decrease in the net accumulation of rubidium ions against a concentration gradient. Superoxide dismutase protected the tissue against this damage. These experiments, therefore, demonstrate the susceptibility of the lens tissue to O2- injury under ambient and nonphotochemical conditions, suggesting a possible implication of this radical in the tissue in vivo and eventual cataract formation. The lumazine/xanthine oxidase system which is known to cause oxygen reduction predominantly by the monovalent route, producing superoxide, appears quite suitable to evaluate the toxicity of O2- to the tissues in vitro.
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PMID:In vitro damage to rat lens by lumazine and xanthine oxidase: prevention by superoxide dismutase. 350 34

The effects of drugs that cause changes in the lens, principally cataractous changes, are discussed. The cataractogenic compounds reported on include 1) drugs used in ophthalmic practice (miotics and topical steroids), 2) compounds used in systemic therapy of a wide range of disorders (corticosteroids andphenothiazines), and 3) compounds that are known to be cataractogenic in animals but not in man (Myleran). Of special interest to family planners is a section on the effects of oral contraceptives on lens changes. Whether long-term use of oral contraceptives would produce ocular complications was queried by Cogan. The influence of these drugs on ocular tissues was subsequently studied, but no significant lens changes were described. Other ocular abnormalities were, however, detected. In rabbit studies, it was shown that mestranol in norethynodrel caused anterior lens changes. Cataracts and other lesions were produced in rats fed a synthetic progestin-estrogen. In vitro changes in lens permeability caused by progestins and progestins and estrogens were demonstrated by Lambert. A dose-dependent increase in rubidium-86 efflux (a measure of lens cell permeability) was demonstrated for several progestins and estrogens. An alteration in cation and water content and lens clarity was also observed. Such physiological changes are similar to those induced by progestins and estrogens in erythrocytes, mitochondria, and lysosomes. It is noted that although the concentrations of drugs used in animals and in vitro studies are high, there is a need for well-controlled, long-term opthalmological studies on women who have chosen oral contraceptives.
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PMID:Effects of drugs on the lens. 494 16

Smoke, either from cigarette smoking or from burning of organic fuels, has been proposed to be a major environmental risk factor for a variety of human diseases. Recently, smoke was implicated in cataract, an eye lens opacification which is a major cause of blindness. We have undertaken a study to investigate the effect of wood smoke condensate on the physiological integrity and morphology of organ cultured lenses. Lenses in organ culture are metabolically active and have functional defense systems, thus they provide an appropriate model for studying effects of smoke condensate. Our present study indicates that metabolites of wood smoke condensate accumulate in the lens. The ability of the lenses to accumulate rubidium-86 (mimic of potassium) and choline from the medium is compromised by exposure to smoke condensate. Rubidium efflux studies suggest that the damage is primarily at the uptake level and does not involve an overall increase in membrane permeability. Protein leakage experiments corroborate this suggestion. Histological data show distinct morphological changes such as hyperplasia, hypertrophy and multilayering of epithelial cells.
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PMID:Effect of smoke condensate on the physiological integrity and morphology of organ cultured rat lenses. 760 15

The prevailing view regarding the mechanism of steroid cataract formation holds that glucocorticoids are covalently bound to lens proteins resulting in destabilization of the protein structure allowing further modification (i.e. oxidation) leading to cataract. Alternative hypotheses (e.g. that cataracts result from glucocorticoid receptor mediated effects) have been difficult to test since protein binding does in fact occur for many cataractogenic steroids. A glucocorticoid lacking the typical glucocorticoid hydroxy group at C21 (fluorometholone, FML), other steroids which can bind to proteins but lack glucocorticoid activity, and a glucocorticoid antagonist (RU486) have been utilized to discriminate between these two hypotheses. Purified bovine beta-crystallin incubated with three different 3H-steroids, dexamethasone (Dex), aldosterone or progesterone demonstrated that the C-21 hydroxyl group is not essential for steroid binding. Progesterone (with no C-21 OH) bound to the greatest extent. Pretreatment of the protein with aspirin to acetylate the free protein amino groups blocked this binding, demonstrating the probability of a Schiff base mechanism. Lens culture studies with the same three radiolabeled steroids demonstrated much the same result. Rat lenses cultured for 48 hr-11 days, demonstrated that loss of GSH is an early and significant effect of several glucocorticoids (Dex, prednisolone and FML) but is not seen with other non-glucocorticoid steroids. However, none of the steroids tested consistently produced lenticular opacification (i.e. cataracts) in this in vitro system, nor did they alter rubidium transport. We suggest that a mechanism other than covalent binding of steroids to lens proteins is responsible for glucocorticoid induced cataracts because: (1) non-glucocorticoids were demonstrated to bind lens proteins as well or better than the glucocorticoid Dex and (2) only glucocorticoids, and not other steroids, lowered lens reduced glutathione content which has been demonstrated to be associated with other forms of cataract.
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PMID:Steroid-induced cataract: new perspective from in vitro and lens culture studies. 946 84

The concentration of taurine is high in the lens. However, its function therein remains unknown. Studies from other tissues suggest that in addition to several other modes of action, it acts as an antioxidant. We therefore hypothesize that taurine may be a part of the antioxidant defense mechanisms involved in protecting the lens against oxidative stress and consequent cataract formation. In these studies, the protective effect of taurine was examined using lens culture system with menadione as an oxidant. Inclusion of this compound in the incubation medium was found to have several adverse effects on the lens, such as a decrease in its ability to accumulate rubidium against a concentration gradient and fall in the levels of glutathione, ATP and an increase in water insoluble proteins. All these deleterious effects were attenuated significantly by addition of physiological amounts of taurine to the menadione-containing medium.
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PMID:Oxidative stress to rat lens in vitro: protection by taurine. 980 50

Data in the present paper demonstrate a significant inhibition in the progress of sugar cataract formation by systemic administration of pyruvate. The formation of the cataract was induced by feeding young rats a diet containing 30% galactose. All animals fed this diet developed nuclear lens opacity by the end of 30 days. This was delayed if the diet and water contained, in addition, 2% sodium pyruvate. The incidence of cataract in the latter group was 0% at day 30 and only 25% at day 55. Physiologically, the inhibition was associated with the prevention of lens membrane damage as reflected by its ability to maintain transport of rubidium ions against a concentration gradient; decreased tissue hydration as indexed by the lens wet weight; inhibition of protein glycation, and higher levels of ATP. Since pyruvate, being a normal tissue metabolite, is likely to be non-toxic, the findings are considered useful for further pharmacological studies with this and other similar metabolites, relevant to protection against various secondary complications of diabetes and galactosemia.
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PMID:Attenuation of galactose-induced cataract by pyruvate. 1023 Aug 4


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