[What possibilities exist to modify cataract development on the basis of current biochemical knowledge? Where can drugs act?].

During the last 10-15 years, investigations into the biology and biochemistry of the lens have demonstrated that the age changes observed cannot be the only cause of the formation of senile cataract. The various types of opacities and the wide age range in which they begin indicate a multifactorial origin involving endogenous and exogenous risk factors. Initial epidemiological studies have identified certain risk factors. Experimental cataract research is able to elucidate possible damaging mechanisms by using cataract models, for instance, the cataracts caused by excess carbohydrate (galactose, glucose), naphthalene application, ionizing rays, or by additional cocataractogenics, thus indicating steps for countermeasures. Taking (true) diabetic cataract of rats after Streptozotocin injection as an example, the efficacy of aldose reductase inhibitors is shown. Even if additional cataractogenic factors such as naphthalene and X-rays are applied, diabetic lens opacities can be prevented completely. Damage by naphthalene is due to an increased oxidative change in the lens protein. Several substances promoting the antioxidative capacity of the lens, thereby inhibiting cataract formation, are already available. Preclinical or clinical studies have demonstrated the efficacy of only a few of the commercially available anticataract drugs. The results of animal experiments presented here may well represent a basis for the development of really effective anticataract drugs.