Cataract in animals

Toxicology. Dimethyl hydrogen phosphite (DMHP) is an irritant of the eyes, mucous membranes, and skin it causes neurological impairment and reversible cataracts in animals it is carcinogenic in rats and causes testicular atrophy in mice. 

Inhibitors of AR have been demonstrated to prevent a wide variety of biochemical, functional and structural alterations in animal models of diabetes. Early studies demonstrated arrest of both early cataract development and nerve conduction velocity. At least 30 clinical trials of AR inhibitors have been published involving nearly 1000 patients in total. However, there is little impressive data of their efficacy up to now but, rather than undermine the hypothesis linking excess polyol pathway activity to diabetic complications, it may reflect methodological difficulties and trial design errors. 

Opaque deposits in the cornea and lens may occur with chronic phenothi-azine treatment, especially with CPZ. Although visual acuity is not usually affected, periodic slit-lamp examinations are recommended with use of long-term phenothiazines. Baseline and periodic slit-lamp examinations are also recommended for quetiapine-treated patients because of cataract development and lenticular changes in animal studies. 

Galactose, if fed in large amounts, causes cataracts in a number of other species, even though the other features of galactosemia are absent. These animal experiments are discussed below (Section 2.7) and enzymic mechanisms possibly related to the development of cataract in Section 3.3.3. 

Practically all of the mercuric compounds are teratogenic in animals [241,242], Mercuric chloride thus induced cataracts and deaths in rat embryos [243]. In the human, mercuric chloride has been related to abortion [244, 245], possibly through the inactivation of placental sulphydryl enzymes. 

The development of cataract in rats by the addition of galactose to the diet can be counteracted during the early stages (first 2 weeks) by the administration of orotic acid [184a]. After 3 to 4 weeks, however, no difference can be seen in the lens opacities between the orotic acid-treated animals and the control [184b-e]. Orotic acid was also reported to be beneficial in human galactosemia [184b,f]. 

Toxicology. Diquat causes gastrointestinal damage, and in animals chronic exposure produces cataracts. 

Rats were exposed at 600, 300, or 100 ppm 6 hours/day 5 days/week for 4 weeks. At the highest dose, severe cataracts developed and 70% of the animals died there was histologic evidence of lung inflammation. The middle dose was lethal to 10% of the exposed group and caused mild cataracts. At the low dose there were mild, reversible striate opacities. In further studies, no effects were observed in animals exposed at 10 ppm. 

Aldose reductase has been implicated in the pathogenesis of cataract in diabetic and galactosaemic animals. The enzyme catalyzes the reduction... 

Lens aldose reductase has been implicated in the pathogenesis of cataracts in diabetic and galac-tosemic animals. The enzyme catalyzes the reduction of glucose and galactose to their polyols, which accumulate in large quantities in the lens and ultimately lead to mature lens opacities. Several key bioflavones have activity against this enzyme. Oral administration of quercitrin decreased the accumulation of sobital in the lens. Therefore, the accumulation of lens opacities could be partially abrogated by certain flavonoids. In a study of 30 flavones, 4 isoflavones, and 13 coumarins, many potent inhibitors were found, but 5,7,3, 4 -tetrahydroxy-3,6-dimethoxyflavone and 6,3, 4 -trihy-droxy-5,7,8-trimethoxyflavone were especially active. 

Ocular effects have not been reported in humans or animals exposed to radium via inhalation, oral, or dermal routes. However, ocular effects have been observed in both humans and animals injected with radium. Cataracts were reported in 6% of the German patients who had been injected with radium-224 as children (Chmelevsky et al. 1988a Stefani et al. 1985). In contrast, the incidence of cataracts in female dial painters was not correlated with total radium intake or age at first exposure, nor was there a difference in appearance times between high and low total radium intakes (Adams et al. 1983). However, the dial painters were exposed orally, the isotope was mainly radium-226, and very few of these dial painters were exposed when younger than 15 years of age. Any of these factors may account for the difference between the results observed in these two studies. 

DNOC causes similar health effects in animals. In addition, injection of other dinitrocresols into animals caused similar effects. High environmental temperatures can worsen the harmful effects in some animals that swallow DNOC. Some animals exposed to DNOC for a long period show blood cell changes. Ducklings given high levels of DNOC in the diet for a short period developed cataracts. 

No reliable animal studies have demonstrated that DNOC causes cataracts in mammals. However, case reports of the coincidental occurrence of cataracts after ingestion of DNOC and the structural similarity between dinitrophenol and DNOC, both of which are uncouplers of oxidative phosphorylation, suggest that this effect may occur in humans exposed to DNOC. 

Cataract has been observed in animals, but even after prolonged use of deferoxamine it has only rarely been reported in humans (63,64). 

Reports of adverse effects following chronic naphthalene exposure include the development of cataracts and retinal hemorrhage in a 44-year-old man occupationally exposed to powdered naphthalene. Unilateral chorioretinitis was reported for a coworker and cataracts developed in 8 of 21 workers exposed to naphthalene fumes or dust for 5 years in an industrial setting. Chronic exposure to powdered naphthalene in the workplace has been associated with an increased incidence of cataracts. However, few of these effects have been confirmed in animal studies. 

S-(l,2-Dichlorovinyl)-L-cysteine (DCVC) is a model nephrotoxicant and cataractogen used to induce acute renal failure and cataracts in experimental animals to study the biochemical, physiological, and molecular mechanisms underlying the disease. 

The effects of DNP found in animals are similar to those in humans, except that the effects on feeling in the hands and feet, and on white blood cells were not found in animals. Cataracts also occurred in some types of animals that swallowed DNP. 

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