Activation of ALDH1A1 by omeprazole reduces cell oxidative stress damage

Under physiological conditions, cells produce low basal levels of reactive oxygen species (ROS); however, in pathologic conditions ROS production increases dramatically, generating high concentrations toxic unsaturated aldehydes. Aldehyde dehydrogenases (ALDHs) are responsible for detoxification these aldehydes protecting the cell. Due to relevance enzymes, it is important design strategies modulate their activity. It was previously reported that omeprazole activation ALDH1A1 protected Escherichia coli overexpressing this enzyme, from oxidative stress generated by H2O2. In work, cell protection potential evaluated eukaryotic cells. AS-30D or hepatocyte suspensions were subjected a treatment with and exposure light (that required activate active site ALDH) then exposed Cells showed viability similar control cells, total activity ALDH preserved, while lipid markers maintained low. Cell avoided inhibition ALDHs disulfiram, revealing key role enzymes protection. Additionally, also preserved ALDH2 (mitochondrial isoform) activity, diminishing aldehyde organelle, mitochondrial respiration transmembrane formation capacity, These results highlight as part antioxidant system cell, since if decreases under compromised.