Effects of mitochondrial poisons on glutathione redox potential and carotid body chemoreceptor activity

We found that rotenone, antimycin A and sodium azide decreased EGSH; NAC restored EGSH to control values

A. Gomez-Niño; M.T. Agapito; A. Obeso; C. Gonzalez


Scholarcy highlights

  • Carotid body chemoreceptor cells and pulmonary artery smooth muscle cells detect hypoxia with a very low threshold generating adaptive responses
  • In the upper and middle panel are shown, respectively, the levels of GSH and GSSG present in the diaphragm in control conditions, in diaphragms incubated with 1 ␮M rotenone and in diaphragms incubated with 1 ␮M rotenone + 2 mM NAC
  • Rotenone 1 ␮M caused a tendency for GSH to decrease to 0.41 ␮mol/g and a tendency for GSSG to increase to 0.021 ␮mol/g
  • Our findings on mitochondrial reactive oxygen species production conform to current literature: blockers of the respiratory chain cause a decrease in EGSH, albeit with different potencies, while the uncoupler did not measurably alter ROS production
  • Selected concentrations of mitochondrial poisons, effective to decrease EGSH, activated CB chemoreceptor cells eliciting the release of neurotransmitters
  • The same doses of mitochondrial poisons caused a decrease of ATP levels in the CB
  • Not addressed in present study, our measurements of ATP would be consistent with the proposal that mitochondrial poisons activation of chemoreceptor cells could be mediated by AMP kinase-dependent inhibition of K+ channels in chemoreceptor cells

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