Coenzyme Q10 reduces sevoflurane-induced cognitive deficiency in young mice

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.

Young mice ( n =134) were randomly assigned into the following four groups: control plus corn oil vehicle (60% oxygen); 3% sevoflurane [2 h daily on postnatal day (P) 6, 7, and 8] plus vehicle; CoQ 10 (50 mg 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.

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.

These data suggest that CoQ 10 reduces sevoflurane-induced cognitive deficiency by mitigating sevoflurane-induced 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.