Catechol inhibits basal respiration in isolated rat brain mitochondria

BARRETO G 1, ALVAREZ LDG 2, OLIVEIRA DM 2, EZEQUIEL SARACENO3, LAURA-AON BERTOLINO3, FRANCISCO CAPANI 3, EL-BACHÁ RS2

Lisboa, Portugal

Congreso; Sociedad de Biologia de Portugal; 2008

Catechol is a metabolite of benzene and spontaneously oxidizes in physiological medium consuming oxygen and forming oxygen species and quinones. To clarify whether catechol could be toxic to the central nervous system, we examined the effects of catechol on the mitochondrial respiratory chain in organelles obtained from freshly rat brain cells. Mitochondria were isolated from brain of adult rats by differential centrifugation. Sodium succinate  was added to a final concentration of 10nM in order to induce mitochondrial basal respiration (state 2) and oxygen consumption was carried out at 37ºC in a closed chamber containing a Clark Type oxygen electrode.  The addition of catechol (1 mM) to brain homogenates resulted in brain mitochondrial inhibition of state 2 FADH2-linked respiration. Catechol decreased O2 uptake by 26% when mitochondrial fractions were obtained immediately after the addition of this compound to brain homogenates (P 0 min). Mitochondrial basal respiration was inhibited by 44% when 1 mM catechol was incubated for 15 minutes with brain homogenates prior to isolation of mitochondria (P 15 min). Presumably catechol inhibits electron flow between Complex II and Complex IV through pathways mediated by phenolic or quinone group substituents on the phenyl ring. These results indicate that catechol inhibits FADH2-linked respiration, suggesting an oxidative pathway implication through the generation of semiquinone and reactive quinones.