Biochemical Lesion of Diphtheria Toxin in the Heart*

Open Access
Publisher Website
Google Scholar
Abstract
Fatty degeneration of the myocardium was induced in guinea pigs with diphtheria toxin. The lesion was expressed biochemically by 1) a depressed rate of long-chain fatty acid (LCFA) and long-chain fatty acyl CoA oxidation, 2) a depletion of carnltine, and 3) an excessive accumulation of trlglycerides. Normal rates of glucose and succinate oxidation demonstrated the integrity of the glycolytic pathway, the Krebs cycle, and the electron transport chain in the hearts exposed to the toxin. Exogenous carnltine had a restorative effect in vitro on the depressed rate of LCFA oxidation in the toxin treated preparations. The observations suggest that 1) diphtheria toxin impedes LCFA oxidation in the heart by interfering with carditine metabolism, and 2) fatty degeneration of the myocardium induced with diphtheria toxin is due to an accumulation of triglyceride synthesized in the heart from fatty acids which cannot be otherwise utilized because of the block in LCFA oxidation.