P Seshagiri Rao
Articles written in Proceedings – Section B
Volume 24 Issue 6 December 1946 pp 264-278
The influence of xanthine, adenine, uric acid, theophylline, guanine, creaturine, oxalic acid, sodium diethyldithiocarbamate and 8-Hydroxy-quinolin on the oxidation of vitamin C by Cu and ascorbic acid oxidase has been studied.
Sodium diethyldithiocarbamate and 8-hydroxyquinolin inhibit both the enzymic and Cu oxidation of vitamin C. The other compounds investigated inhibit only the Cu oxidation without exerting any influence on the enzymic oxidation of the vitamin.
The bearing of these results on the nature of ascorbic acid oxidase and their application to the study of the nature of catalytic systems in plants which oxidise the vitamin have been discussed. Various types of inhibitors of vitamin C oxidation have been listed and properly classified.
Volume 28 Issue 2 August 1948 pp 71-82
The mechanism of the β-amylase inhibition by Vitamin C has been further critically examined. The observed inhibition of the hydrolysis of starch by Vitamin C alone may be due to adsorption or complex formation of the Vitamin with the substrate, the modified substrate thus formed being less easily hydrolysed than the free starch.
Dehydroascorbic acid has no effect on the hydrolysis of starch by the amylase as well as on the enzyme in the absence of the substrate.
Hydrogen peroxide alone does not inhibit the hydrolysis of starch, but in the presence of Cu it exerts a feeble inhibition of the hydrolysis.
The inhibition of the amylolytic hydrolysis of starch by the oxidized products of Vitamin C by Cu oxidation, is mainly due to the traces of cuprous oxide formed during the oxidation of the vitamin.
The protective factor present in the β-amylase is found to be undialysable and thermostable.
Volume 30 Issue 6 December 1949 pp 316-330
Vitamin C, copper and vitamin C—Cu complex had no inhibitory effect on prothrombin activity, the lack of inhibition being due to the stabilization of the vitamin by the protective factors associated with the enzyme.
While hydrogen peroxide had no effect on prothrombin activity, iodine and sodium thiosulphate were found to inactivate prothrombin, the activity in both the cases being regenerated by passing carbon dioxide. Reducing agents like sodium sulphite, however, did not regenerate the prothrombic activity lost by treatment with iodine.
The organic solvents, chloroform and carbon tetrachloride were found to have neither activating nor inhibiting effect on prothrombin.
The presence of traces of fibrinogen along with prothrombin appears to be necessary for the stability of the enzyme.
The results have an important significance in throwing new light on the nature of the prothrombin and the mechanism of blood coagulation.
Volume 30 Issue 6 December 1949 pp 331-337
Lucerne loses more than 80% of its vitamin C on drying either in direct sunlight or under the fan at 25° C.
Lucerne contains a feeble oxidase system and a powerful protective factor, which is very thermostable and which is associated partly with the colloidal and dialysable portions of the juice.
The protective factor is isolated free from the oxidase system and it is found to annul the non-cupric and cupric ion oxidation of vitamin C, without having any effect on the enzymic oxidation of the vitamin.
Volume 35 Issue 3 March 1952 pp 132-142
Vitamin C and Vitamin C-Cu complex inhibit urease activity, the inhibition being very marked in the latter case.
The inhibition of urease activity of Vitamin C is not due to dehydro-ascorbic acid as the degree of inhibition produced by it is negligible compared to that produced by Vitamin C at equal concentration.
A variety of compounds other than cysteine, like 8-hydroxy-quinoline, sodium-diethyl-dithio-carbamate and potassium cyanide, which are known to protect Vitamin C against oxidation catalysed by Cu++, are shown to protect the urease from inactivation by Vitamin C and Vitamin C-Cu. showing that the inactivation of urease by Vitamin C is related to the oxidation of the vitamin.
A well marked correlation between the inactivation of urease on the one hand and the oxidation of Vitamin C on the other has been established.
It is suggested that the inactivation of urease by Vitamin C catalyzed by Cu++ may be due to any intermediate products like Cu2O formed during the oxidation.