It was found that two chemically very close Non-Steroid Antiinflammatory Drugs (NSAID), bendazac and benzydamine, were able to reduce the Biological Liquid Oxidant Activity (BLOA) in vitro (bendezac) and in vivo (bendazac and benzydamine). Four hundred and seven patients were treated with bendazac and 599 with benzydamine. After a single dose oral administration they effected a BLOA Reducing Activity (BRA) ranging from 5% to over 20% in about 40% of cataractous patients. When these drugs were able to reduce the BLOA, they showed anticataract activity in about 50% and about 90% of patients according to the extent of BRA, i.e., less than 20% and greater than or equal to 20% of the basal value. This fact suggests that the anticataract agent is not the original NSAID (prodrug) but a NSAID metabolite or an elicited endogenous compound which produced the BLOA reduction. Individual BLOA could be reduced in vivo by benzydamine or bendazac, by both or by neither of them. This finding may be accounted for by selective biotransformation of each patient's original NSAID into the antioxidant anticataract compound. However, other possible mechanisms of the anticataract activity beside antioxidant activity might take place, such as protein and membrane stabilization, together with a not yet defined activation of enzymes within the lens effecting the reversal of cataractous opacity. Several side effects were apparent in short and long term treatments. The final conclusion of our study is that bendazac at a dosage ten-fold lower than that used in the clinics is anticataract drug when orally administered to "BLOA test selected" patients, at least for short term treatment of young, otherwise healthy humans with cortical cataract.