A possible mechanism of X-ray-induced injury in rat lens.

PURPOSE: X-ray and other radiation can cause cataract, but the pathogenic mechanism is largely unknown. The aim of this study was to investigate the accumulation of iron in the x-ray-exposed rat lens and its relationship to lens injury. METHODS: Fifty male Wistar rats were divided randomly into five groups of 10. Groups 2 and 4 rats were sham-exposed, groups 3 and 5 were x-ray-treated, and group 1 served as control. X-ray radiation and sham exposure were performed in a similar manner. After 10 and 30 days of exposure, a lens from each rat in groups 2 and 3, and 3 and 5, respectively, were analyzed by flame atomic absorption technique for the assessment of metal content. RESULTS: Significantly decreased zinc and increased iron and calcium concentrations were detected in the lens samples of groups 3 and 5 compared with groups 2 and 4 and controls. Similar results were obtained comparing groups 5 and 3. CONCLUSIONS: We propose that x-ray exposure may cause toxic cell injury of the rat lens via Fenton metals catalyzed damage. Initial lens membrane damage in the radiolytic phase may permit the access of iron resulting in lens damage.

The role of erythrocyte protoporphyrin in the diagnosis of iron deficiency anemia of children.

The values of erythrocyte protoporphyrin, ferritin and mean corpuscular volume (MCV) measurements in diagnosing iron deficiency anemia were investigated in 72 iron deficient and in 25 healthy control infants. Receiver operator curve, sensitivity and specificity of erythrocyte protoporphyrin, ferritin and mean corpuscular volume were compared between the study and control groups. In the study group mean corpuscular volume, hemoglobin and ferritin concentrations were significantly lower, and erythrocyte protoporphyrin was significantly higher when compared to the control group. In the iron deficient study group, erythrocyte protoporphyrin was the most sensitive test and ferritin was the most specific test, whereas ferritin was the most diagnostic test and mean corpuscular volume was the least diagnostic test. A significant correlation between erythrocyte protoporphyrin and hemoglobin values was determined. We conclude that erythrocyte protoporphyrin is a more sensitive but less specific test than ferritin, and it can be used as a first-line diagnostic test in the evaluation of iron deficiency and in diagnosing iron deficiency anemia in infants.

Cataractous changes in rat lens following cigarette smoke exposure is prevented by parenteral deferoxamine therapy.

OBJECTIVES: To test whether iron accumulation in the lens following cigarette smoke exposure is the principal mechanism in smoke-related cataractogenesis and to assess the possible protective effect of deferoxamine mesylate treatment against lenticular degeneration with in vivo exposure to cigarette smoke. METHODS: Thirty-two male Wistar rats were randomly divided into 4 equal groups. Groups 3 and 4 rats were exposed to cigarette smoke for 1 hour each day for 90 consecutive days, and groups 1 and 2 rats were treated in a similar manner but exposed only to room air. In addition, deferoxamine was given subcutaneously to groups 2 and 4 rats. Both eyes of all the animals were then enucleated and 1 eye prepared for histopathological examination. The fellow eye was used to measure iron, calcium, zinc, and copper levels. RESULTS: Significantly higher iron and calcium and lower zinc levels were observed in the lenses of group 3 rats compared with those in the other groups. Similar comparisons performed between groups 1 and 2, 1 and 4, and 2 and 4 did not show any significant difference. Copper concentrations did not differ between groups. Distinct histopathological changes in the anterior lens epithelium, such as hyperplasia, hypertrophy, and epithelial multilayering, and the presence of swollen epithelial cells overlying the posterior lens capsule, observed in group 3 rats, were not present in the other groups. CONCLUSIONS: Cataractogenesis following cigarette smoke exposure in rats was associated with the accumulation of iron, and concurrent deferoxamine therapy prevented such cataract formation. CLINICAL RELEVANCE: Our results may apply to human cataract formation associated with cigarette smoking, so such pathogenesis may be prevented by concurrent parenteral deferoxamine treatment. Clinical studies are needed, however, to determine the value of this suggestion.

Cadmium and iron accumulation in rat lens after cigarette smoke exposure and the effect of vitamin E (alpha-tocopherol) treatment.

PURPOSE: Cadmium accumulation in the lens has been implicated in cataractogenesis of chronic smokers. This study was planned to evaluate whether or not in vivo cigarette smoke exposure causes cadmium accumulation in rat lens, and possible protective effect and mechanism of alpha-tocopherol (vitamin E) treatment on cataractogenesis. METHODS: 28 male Wistar rats were randomly divided into four equal groups. Group 3 and 4 rats were exposed to cigarette smoke over ninety consecutive days, and Group 1 and 2 rats were treated in a similar fashion but exposed only to room air. Additionally, vitamin E was given to Group 2 and 4 rats. RESULTS: Significantly higher iron levels were observed in the lenses of Group 3 rats compared to other groups. With respect to cadmium, Group 3 and 4 rats had significantly higher levels compared to Group 1 and 2 rats. Although vitamin E treatment prevented iron accumulation in Group 4 rats, it had no effect on cadmium concentrations. Distinct histopathological changes observed in Group 3 rats were not present in Group 4 rats. CONCLUSION: Our study demonstrates that in vivo cigarette smoke exposure causes accumulation of cadmium in rat lens and IM vitamin E treatment does not affect this accumulation. The protective effect of vitamin E treatment on smoke exposed rat lens seems to be mediated by blockage of iron accumulation in the lens.

Prevention of lens damage associated with cigarette smoke exposure in rats by alpha-tocopherol (vitamin E) treatment.

PURPOSE: To evaluate the possible protective effect and mechanism of alpha-tocopherol (vitamin E) treatment on lens degeneration associated with in vivo exposure to cigarette smoke and to further clarify the role of iron in cigarette smoke-generated lens damage. METHODS: Twenty-eight male Wistar rats were randomly divided into four equal groups. Rats in groups 3 and 4 were exposed to cigarette smoke for 1 hour each day over 90 consecutive days, and rats in groups 1 and 2 were treated in similar fashion but only exposed to room air. Additionally, vitamin E was given to the rats in groups 2 and 4 via intramuscular route. At the end of the study, both eyes of all the animals were enucleated; one eye was prepared for histopathologic examination, and the fellow eye was used for the measurement of iron and calcium levels. RESULTS: Significantly higher iron and calcium levels were observed in the lenses of group 3 rats than in other groups. Similar comparisons performed between groups 1 and 2, groups 1 and 4, and groups 2 and 4 did not show any significant difference. Distinct histopathologic changes in the anterior lens epithelium, such as hyperplasia, hypertrophy, epithelial multilayering, and the presence of epithelial cells over posterior lens capsule, observed in group 3 rats were not present in other groups. CONCLUSIONS: Cataractogenesis after cigarette smoke exposure was associated with an accumulation of iron and calcium in the rat lens, and vitamin E supplementation protected such accumulations and cataractogenesis.

Determinations of some trace and heavy metals in rat lenses after tobacco smoke exposure and their relationships to lens injury.

Cigarette smoking has been implicated in the pathogenesis of cataract, but the pathogenic mechanism by which cigarette smoke causes cataract is yet to be completely understood. There has been suggestion that oxidative damage caused by accumulation of Fenton reagents (iron and copper) in the lens can cause lens damage and possibly cataract. To investigate the accuracy of this theory the study was planned. A number of twenty-four male Wistar rats were divided randomly into experimental and control groups. The experimental group of rats were exposed to cigarette smoke for two hours in each day over sixty consecutive days and the controls were treated in identical fashion but only exposed to room air. At the end of the study period, both eyes of all the animals were enucleated and one eye prepared for histopathological examination and the other used for the measurement of metal levels. The lenses of experimental animals showed significantly decreased zinc and increased iron, and calcium concentration relative to those of sham exposed controls. However, no significant difference was found in the copper contents of the lenses of both groups. Distinct histopathological changes such as hyperplasia, hypertrophia, and multilayering of epithelial cells and elevations of calcium concentration detected in the lenses of experimental group animals suggested that the lens damage was a result of in-vivo exposure to tobacco smoke. We propose that increased metal contents in the lens can cause lens damage by the mechanism of oxidative stress through formation of oxygen radicals via metal catalysed Fenton reaction.