The Effect of Nicotinamide Adenine Dinucleotide and Rotenone on the Oxidation of Choline by Rat Liver Mitochondria

• Published in: The Journal of biological chemistry Vol. 242; no. 20; pp. 4614 - 4618
• Main Authors: Feinberg, R H, Turkki, P R, Witkowski, P E
• Format: Journal Article
• Language: English
• Published: United States American Society for Biochemistry and Molecular Biology 25.10.1967
• Subjects: Aldehydes - metabolism; Animals; Betaine - metabolism; Choline - metabolism; Depression, Chemical; Feedback; Manometry; Mitochondria, Liver - metabolism; NAD - pharmacology; Oxidation-Reduction; Rats; Rotenone - pharmacology; Semicarbazides - pharmacology; Stimulation, Chemical
• ISSN: 0021-9258; 1083-351X
• DOI: 10.1016/S0021-9258(18)99501-3

The effect of semicarbazide on the oxidation of choline by rat liver mitochondria was studied. Semicarbazide was used to prevent both further oxidation of betainealdehyde and product inhibition of choline dehydrogenase by the aldehyde. NAD did not stimulate choline-based respiration when semicarbazide was present to prevent the oxidation of enzymatically formed betainealdehyde. In contrast, NAD did stimulate respiration when the semicarbazide was omitted. NAD stimulation of choline-supported respiration appears to be entirely due to its effect on the oxidation of betainealdehyde. In both the presence and the absence of semicarbazide, rotenone inhibited the oxidation of choline. It was concluded that the rate of choline oxidation to betainealdehyde is decreased by rotenone and that this inhibition is not due to product inhibition by betainealdehyde. Choline oxidation by submitochondrial particles was insensitive to rotenone. Inhibition of respiration by rotenone was found to be competitive with respect to choline. Acetate ion eliminated the rotenone sensitivity of choline oxidation. These results suggest that rotenone may inhibit choline oxidation by reducing the rate of entry of choline into intact mitochondria.