Effect of rifampicin and erythromycin on the initiation of galactose induced cataract in rats

Cataract is the leading cause of blindness with a number of risk factors such as aging, genetic, steroids, nitric oxide, diabetes, ultraviolet radiation and smoking. An increased incidence of cataract is associated with diabetes and it is one of the major cause of visual impairment in diabetics. Cataractogenesis is one of the earliest secondary complications of diabetes mellitus. The mechanism involved in the development of diabetic cataract is different from senile cataract. The accumulation of polyols within the lens is an important contributing factor in diabetic cataractogenesis. The enzyme aldose reductase within the lens converts glucose to sorbitol or galactose to galactitol using NADPH as a co-factor. Electron transfer from NADPH further depends on cytochrome P450 (CYP) system. These polyols thus formed, accumulate and lead to the formation of cataract. It has thus been hypothesized that by using enzyme inducer, pioglitazone, and inhibitor, diltiazem and nifedipine, the activity of aldose reductase and formation of cataract can be altered. However Jaykaran and Mahajan et al. have questioned the inclusion of pioglitazone, a weak inducer of CYP enzyme. The present study was undertaken to test the role of rifampicin, known cytochrome inducer and erythromycin, known cytochrome inhibitor on the development of cataract based on the above hypothesis.