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Physiology and Biochemistry

Inhibition of Respiration in Pythium Species by Ethazol. Ponciano M. Halos, Former Graduate Student, Department of Plant Pathology, University of California, Berkeley 94720, Present address of senior author: Department of Plant Pathology, University of the Philippines, Los Baños, Laguna, Philippines; O. C. Huisman, Assistant Professor, Department of Plant Pathology, University of California, Berkeley 94720. Phytopathology 66:158-164. Accepted for publication 18 August 1975. DOI: 10.1094/Phyto-66-158.

Ethazol [5-ethoxy-3-(trichloromethyl)-1,2,4-thiadiazole] concentrations that inhibited growth also proportionately decreased respiration in Pythium debaryanum, P. ultimum, P. sylvaticum, and P. vexans. Time-course studies revealed that 18 µM of the chemical inhibited growth in culture by 50% after 4 hours. While glucose and acetate oxidations were relatively insensitive, those of succinate and malate were inhibited 50% after only 3 hours of treatment. Since the uncoupler dinitrophenol did not reverse ethazol inhibition, the fungicide does not interfere with oxidative phosphorylation. Evidence suggested a block in the electron transport system. Tetramethyl-p-phenylenediamine reversed the inhibition indicating that the site of ethazol inhibition is between cytochromes b and c. Cysteine and ascorbic acid also reversed ethazol inhibition of oxygen uptake. The site of ethazol action was verified in isolated mitochondria from Pythium species. In P. ultimum, ethazol (18 µM) reduced NADH and succinate oxidations by 50% after 1 minute. The proximity or identity with the antimycin-inhibited site was demonstrated in Pythium species and beef heart mitochondria. Mitochondrial respiration in Fusarium oxysporum f. sp. vasinfectum, pinto bean, and beef heart was much more resistant to ethazol inhibition than that in Pythium species. Differential sensitivity to respiratory inhibition may therefore account for selectivity of ethazol.