Dexmedetomidine protects blood δ-aminolevulinate dehydratase from inactivation caused by hyperoxygenation in total intravenous anesthesia

Abstract

Delta-aminolevulinate dehydratase (δ-ALA-D) enzyme is sensitive to pro-oxidant agents, including molecular oxygen. Here, we tested whether hyperoxygenation after total intravenous (i.v.) anesthesia could interact with the type of anesthesia (dexmedetomidine, continuous infusion; 0.5 μg/kg/h or remifentanil, continuous infusion; 0.3 μg/kg/min) plus propofol using blood δ-ALA-D activity and thiobarbituric acid reactive substances (TBARS) levels as ending points of toxicity. In absence or presence of dithiothreitol (DTT), δ-ALA-D activity was reduced after hyperoxygenation in the group treated with remifentanil and was not modified in dexmedetomidine group. TBARS increased considerably in the blood of both groups of patients after oxygenation. The results obtained here suggest that the hyperoxygenation was associated with a marked increase in TBARS production regardless of the type of anesthesia. δ-ALA-D activity was only inhibited in remifentanil group, which indicates a possible interaction between oxygenation and the type of anesthetic. This is the first demonstration that dexmedetomidine may protect blood δ-ALA-D from oxidation. However, further studies are necessary to establish a possible antioxidant role of dexmedetomidine against hyperoxygenation in human blood.