Abstract
d-Glucose-supported O 2 uptake in the filarial nematode Brugia pahangi was partially inhibited by antimycin A (30–40%), with the remaining activity being sensitive to o-hydroxydiphenyl or salicylhydroxamic acid (SHAM). The production of CO 2 by B. pahangi in the presence of d-glucose was stimulated by O 2; the stimulation of CO 2 production was sensitive to antimycin A. The O 2 dependencies of respiration showed that the apparent O 2 affinity for B. pahangi was diminished in the presence of antimycin A; O 2 thresholds for inhibition of respiration were observed which showed that the alternative electron transport pathway was less sensitive to inhibition at elevated O 2 concentrations. H 2O 2 production and its excretion could be detected in whole B. pahangi; higher rates were observed in the presence of the uncoupler carbonyl cyanide m-chlorophenylhydrazone. The effects of inhibitors on H 2O 2 production suggest two sites of H 2O 2 production, one associated with the classical antimycin A-sensitive pathway, the other with the alternative respiratory pathway. The similarity in the O 2 dependencies of H 2O 2 production and respiration may indicate that H 2O 2 production is involved in O 2-mediated toxicity. Succinate and malate respiring sub-mitochondrial particles of B. pahangi produced O 2 .− radicals at a site on the antimycin A-sensitive respiratory pathway. Inhibition of the alternative electron pathway by SHAM was unusual; sub-millimolar concentrations markedly stimulated respiration, H 2O 2 production and O 2 .− production by 30,20 and 25%, respectively, whereas higher concentrations (> 2.5 m m) inhibited respiration by 75% and H 2O 2 and O 2 .− production by up to 85%.
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