Anesthesia has been linked to oxidative stress, which is the result of reactive oxygen species (ROS), often in the form of free radicals, attacking biomolecules, such as the lipids that make up a cell's membrane. As the lipids are oxidized, the cell membrane loses its integrity resulting in cell death, which is hypothesized to lead to memory loss (Senoner et al., 2021); however, the molecular mechanism by which anesthetics affect cell death in unknown. Three possible mechanisms are proposed by which anesthetics could cause lipid oxidation: by acting as a catalyst and speeding up the oxidation rate, by acting as an adduct and directly reacting with the lipids, or by acting as an initiator for the overall oxidation reaction. Based on data collected from reacting ether and the common anesthetics sevoflurane and propofol individually with linoleic acid (a lipid that constitutes a portion of the cell membrane), the results indicated that all the anesthetics oxidize linoleic acid. The oxidation of linoleic acid was monitored by UV-Vis spectroscopy, showing an increase in the formation of conjugated systems, indicated at wavelength 232nm, which is a sign of oxidation. Additional UV-Vis experiments were run to determine if the anesthetics were acting as a catalyst by measuring the rate of conjugation at 232 nm at two concentrations of linoleic acid. Using a lipid hydroperoxide assay, linoleic acid showed increased hydroperoxide concentration in the presence of an anesthetic when compared to linoleic acid alone, an indication of further oxidation or adduct formation. Through these methods, three possible mechanisms were proposed that demonstrate how different types of anesthesia oxidize lipids, allowing for a possible explanation for memory loss.
