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As is well known, L-ascorbic acid (AA) is catalytically oxidized in the presence of Cu". It is also known that acidic chelating agents, such as EDTA, have an inhibitory effect on this oxidation reaction, whereas basic chelating agents, such as ethylene diamine (EDA) , have an accelerating effect. Both the inhibition and the acceleration are considered to be due to chelation with Cu-" . The author reported in a previous paper (1) that kanamycin (KM), a basic antibiotic, formed a soluble Cu" chelate . Hence, it was thought that KM should accelerate the above oxidation reaction. To test this, the rate of the oxidation reaction of the AA Cu++ system was measured in the absence and presence of KM. The effect of another basic antibiotic, dihydrostreptomycin (DH SM), which is known to form a Cu++ chelate was also tested. The standard reaction mixture consisted of 0.02 mg,/ml of AA, 8 x 10' M of CuC12 and 4 x 10 M of antibiotic or chelating agent in a total volume of 50 ml. The mix ture was adjusted to pH 8.0 with NaOH. A control containing no antibiotic was always incubated simultaneously. The reaction mixtures were incubated at 45.0`C and the time-course of the decrease in the conteni of AA was measured at 20 minute intervals by the standard titration method with 2,6-dichlorophenol indophenol. Fig. 1 shows a comparison of the accelerating activities of KM, DHSM, EDA and guanidine. It is clear that KM caused the highest acceleration of the oxidation of AA catalyzed by Cu-"-,*. The effect of EDA was relatively high, whereas those of DHSM and guanidine were low. KM formed a chelate with Cu++ mainly through its two amino groups of the deoxystreptamine moiety and there fore the structural resemblance of KM to EDA was greater than with DHSM. Since DHSM has been

ACCELERATING EFFECT OF Cu++ CHELATE OF KANAMYCIN ON OXIDATION OF L-ASCORBIC ACID