Mitsutaro Akao

Inactivation of rifampin by Nocardia brasiliensis.

Rifampin was glycosylated by a pathogenic species of Nocardia, i.e., Nocardia brasiliensis. The structures of two glycosylated compounds (RIP-1 and RIP-2) isolated from the culture broth of the bacterium were determined to be 3-formyl-23-(O-[beta-D-glucopyranosyl])rifamycin SV and 23-(O-[beta-D-glucopyranosyl])rifampin, respectively. Both compounds lacked antimicrobial activity against other gram-positive bacteria as well as the Nocardia species.

Metabolic degradations of nitrofurans by rat liver homogenate.

Abstract The evidence of the metabolic degradations of some nitrofurans by rat liver homogenate was shown in the present study. Nitrofurans were incubated with 8500 g supernatant of rat liver homogenate with added NADPH 2 as a hydrogen donor and metabolic degradations of nitrofurans were followed by the changes of their characteristic optical absorbances and the loss of their nitro groups. These two properties of most of the tested nitrofurans changed slowly and independently in aerobic condition. In anaerobic condition, they disappeared much more rapidly and nearly to the same extents.

Reduction by fumaric acid of side effects of mitomycin C

Abstract The toxic symptoms in ICR mice given mitomycin C (either successive daily i.p. doses of l mg kg or two large doses of 4 mg kg ) were reduced by the concurrent administration of fumaric acid (40 mg kg ). Fumaric acid did not reduce the antitumor activity of mitomycin C against either the solid or the ascitic form of the Ehrlich tumor. Fumaric acid reduced the lethal and hematologie toxicities of mitomycin C, and studies on the nucleic acids of animal tissues indicated that mitomycin C inhibited selectively DNA synthesis of liver and kidney, whereas fumaric acid exerted an enhancing effect, antagonistic to mitomycin C, on DNA synthesis of these tissues.