Coenzyme Q10 (
CoQ10,
ubiquinone) is a highly mobile electron carrier in the mitochondrial respiratory chain that also acts as an
antioxidant. We evaluated the cardiovascular protective efficacy of
CoQ10 at the rostral ventrolateral medulla (RVLM), a medullary site where sympathetic vasomotor tone originates and where the
organophosphate poison mevinphos (Mev) acts to elicit cardiovascular intoxication. Experiments were carried out in adult male Sprague-Dawley rats that were maintained under
propofol anesthesia. Microinjection bilaterally of Mev (10 nmol) into the RVLM induced progressive
hypotension and minor
bradycardia, alongside significant depression of the activity of
NADH cytochrome c reductase (
enzyme marker for Complexes I and III) or
cytochrome c oxidase (
enzyme marker for Complex IV) in the mitochondrial respiratory chain, reduction in
ATP concentration, or tissue
hypoxia in the RVLM. On the other hand, the activity of
succinate cytochrome c reductase (
enzyme marker for Complexes II and III) remained unaltered. The Mev-
induced hypotension, bioenergetic failure, or
hypoxia was significantly reversed when
CoQ10 (4 microg) was coadministered bilaterally into the RVLM with the
organophosphate poison. We conclude that
CoQ10 confers cardiovascular protection against acute Mev intoxication by acting on the RVLM, whose neuronal activity is intimately related to the "life-and-death" process. We also showed that amelioration of the selective dysfunction of respiratory
enzyme Complexes I and IV in the mitochondrial respiratory chain, the reduced
ATP level, and the induced tissue
hypoxia in the RVLM are among some of the underlying mechanisms for the elicited protection.