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Anticoagulant Effects of Antioxidant Capacity

In response to the paper by Goode et al) we support some of their findings and offer an alternative explanation. They demonstrated differences in antioxidant capacity in plasma, dependent on the choice of anticoagulant used. They are unsure whether this is due to heparin increasing the antioxidant capacity or to EDTA having a reducing effect. Comparison with serum from these subjects may help. We have compared serum with heparinized and EDTA plasma using the enhanced chemiluminescence (ECL) assay," one of the assays they studied. This data suggest that a reduction in antioxidant capacity by EDTA is more likely; comparison of EDTA plasma with serum gave lower results (352'8 ± 65·9 versus 402·4 ± 49'4uM, P 0,05, n = 10). The suggestion that heparin may be stimulating release of superoxide dismutase (SOD) from endothelial cells seems unlikely, if as implied in the paper, heparin is only in contact with the blood after sampling, rather than from an infusion. The possibility that heparin is affecting release of SOD from red cells cannot be ruled out, but our experience is that metallo-enzymes do not contribute to the ECL assay. This also makes it unlikely that EDTA is exerting a negative effect through metallo-enzymes. Their point that EDTA has a negative effect on retinol, vitamin E and p-carotene results, when measured by liquid choromatography is a valid one. However, due to the relatively low concentrations of these compounds in plasma we feel that this is unlikely to fully account for the differences observed. It may be possible that EDTA is reducing urate, which is the major contributor in the ECL assay. Others have found that the presence of EDTA as an anticoagulant is associated with significantly lower levels of uric acid and vitamin A.3 This may be due to the potential of EDTA to act as a pro-oxidant in combination with iron." The time period of exposure of erythrocytes to