Dipyridamole and RA‐642 Inhibit the Production of Superoxide Anion and Free Radical Damage to Rat Lens

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Abstract
We studied the effects of dipyridamole and RA‐642 on the production of superoxide anions and on oxygen radicals‐induced lipid peroxidation in lens tissue homogenates from normal rats and rats given dipyridamole or RA‐642 intraperitoneally. Superoxide production was evaluated by phenazine methosulphate (PMS)‐induced nitroblue tetrazolium (NBT) reduction and lipid peroxidation by ferrous sulfate and ascorbic acid (FeAs)‐induced malondialdehyde (MDA) production. Dipyridamole and RA‐642 showed an inhibitory effect on both assays in the experiments with lens tissue homogenates from untreated or treated rats. The extent of inhibition, however, was significantly higher in pyrimidopyrimi‐dinic‐treated rats (range of inhibition at different times of incubation was 18% versus 23–57. for dipyridamole and 14% versus 73–80. for RA‐642 in the assay of MDA production, and 10% versus 33–37. for dipyridamole and 2.5% versus 11–32. for RA‐642 in the assay of NBT reduction). Concentrations of dipyridamole and RA‐642 in lens tissue from treated animals could not be determined (< 0.001 μg/mg of tissue). Although both compounds inhibited lipid peroxidation induced by oxygen free radicals, the mechanism of action might include the role of adenosine as a mediator.
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