-1(1).png)
.png)
.png)
ABSTRACT
Biochemical evidence suggests that oxidative damage of the lens proteins is involved in the genesis of senile cataract and the degenerative manifestations of diabetes such as diabetic cataract. This damage either decreases the antioxidant capacity or decreased antioxidant capacity results in oxidative damage. To test this hypothesis the antioxidant status in senile (n = 26) and diabetic (n=18) cataractous lenses was investigated by determining Cu, Zn-superoxide dismutase (Cu, Zn-SOD) and catalase activities by enzymatic and colorimetric methods respectively. Both Cu, Zn-SOD and catalase levels were significantly lower in the diabetic cataractous lenses. The following results were obtained: (mean ± SEM, diabetic and senile cataractous lenses respectively) Cu, Zn-SOD 8.052 ± 0.428 (micro/g prot. and 18.216 ± 0.827 (micro/g prot. (p < 0.05); catalase 0.326 ± 0.031 kU /g prot. and 0.665 ± 0.063 kU /g prot. p<0.001). The decreased activities pointed to a decrement of the antioxidant capacity in the diabetic cataractous lenses suggesting the implication of antioxidant enzymes in the genesis of diabetic cataract.
Biochemical evidence suggests that oxidative damage of the lens proteins is involved in the genesis of senile cataract and the degenerative manifestations of diabetes such as diabetic cataract. This damage either decreases the antioxidant capacity or decreased antioxidant capacity results in oxidative damage. To test this hypothesis the antioxidant status in senile (n = 26) and diabetic (n=18) cataractous lenses was investigated by determining Cu, Zn-superoxide dismutase (Cu, Zn-SOD) and catalase activities by enzymatic and colorimetric methods respectively. Both Cu, Zn-SOD and catalase levels were significantly lower in the diabetic cataractous lenses. The following results were obtained: (mean ± SEM, diabetic and senile cataractous lenses respectively) Cu, Zn-SOD 8.052 ± 0.428 (micro/g prot. and 18.216 ± 0.827 (micro/g prot. (p < 0.05); catalase 0.326 ± 0.031 kU /g prot. and 0.665 ± 0.063 kU /g prot. p<0.001). The decreased activities pointed to a decrement of the antioxidant capacity in the diabetic cataractous lenses suggesting the implication of antioxidant enzymes in the genesis of diabetic cataract.