Coenzyme Q10 reduces sevoflurane-induced cognitive deficiency in young mice

Background. Anaesthesia can induce cognitive deficiency in young rodents and monkeys. Mitochondrial dysfunction contributes to the anaesthesia-induced neurotoxicity and neurobehavioural deficits. We therefore assessed the effects of the mitochondrial energy enhancer coenzyme Q(10) (CoQ(10)) on anaesthesia-induced cognitive deficiency in young mice to investigate the role of mitochondrial dysfunction. Methods. Young mice (n = 134) were randomly assigned into the following four groups: control plus corn oil vehicle (60% oxygen); 3% sevoflurane [2h daily on postnatal day (P) 6, 7, and 8] plus vehicle; CoQ(10) (50mg kg(-1)) plus vehicle; or 3% sevoflurane plus CoQ(10) plus vehicle. We determined cognitive function using the Morris water maze at P31-P37. We quantified brain postsynaptic density protein-95, the presynaptic marker synaptophysin, adenosine triphosphate, reactive oxygen species, and mitochondrial membrane potential at P8 and P37. Results. Coenzyme Q(10) reduced sevoflurane-induced cognitive deficiency in young mice (F = 0.90, P = 0.49, n = 10-16) and attenuated sevoflurane-induced reductions in postsynaptic density protein-95 (F = 10.56, P< 0.01, n = 6), synaptophysin (F = 8.44, P = 0.01, n = 6), adenosine triphosphate (F = 4.34, P = 0.05, n = 9), and mitochondrial membrane potential (F = 11.43, P< 0.01, n = 6), but not sevoflurane-induced increases in reactive oxygen species (F = 1.17, P = 0.20, n = 6), in brain. Conclusions. These data suggest that CoQ(10) reduces sevoflurane-induced cognitive deficiency by mitigating sevofluraneinduced mitochondrial dysfunction, the reduction in adenosine triphosphate, and synaptic dysfunction. Coenzyme Q(10) could provide an approach to reduce the neurotoxicity of anaesthesia in the developing brain.