Abstract
Malic dehydrogenase activity of the kidney homogenate from the normal and the tuberculous guinea pigs has been estimated. A defect in the electron transport chain has been detected at the level of flavoprotein-diaphorase system. A significantly high DPNase activity of kidney homogenate has also been found in the infected group. Niacin and phenazine methochloride could correct both the defects and improve the tetrazolium reduction of the homogenate in the infected group to the level of the normal activity. Oxidative phosphorylation by the kidney mitochondria from the tuberculous guinea pigs was found to be low and could not be improved by niacin and phenazine methochloride, unlike their effects on the reduction of tetrazolium. Results have been discussed in the light of the over-all intercellular economy and its relation to the symptom complexes in tuberculosis.
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