Effect of Bordetella endotoxin upon mitochondrial respiration and energized processes

Endotoxin isolated from Bordetella bronchiseptica 22067 by the Boivin method markedly affected respiration, certain energized processes, and the morphology of beef-heart mitochondria. Interaction of endotoxin with intact mitochondria resulted in loss of respiratory control, inhibition of the coupling of phosphorylation to terminal electron transfer, inhibition of respiration in presence either of DPNH-linked substrates or of succinate, stimulation of respiration with ascorbate-TPD⁴ as electron donor, inhibition of Ca²⁺ translocation whether energized by electron transfer or by ATP, but stimulation of Mg²⁺ translocation energized by ascorbate plus TPD. Changes in the morphology of the inner membrane as a result of interaction of the mitochondrial membrane system with endotoxin were readily demonstrable. A submitochondrial preparation composed predominantly of inner membrane (ETP_H) was much more resistant than intact mitochondria to the action of endotoxin; higher concentrations of endotoxin were necessary for inhibition of respiration and energized processes. The action of B. bronchiseptica 22067 endotoxin mimicked, in part, that of other reagents, such as the murine toxin of Pasteurella pestis, Zn²⁺, certain basic proteins, and parathyroid hormone.