Cells are equipped with versatile physiological stress responses to prevent hazardous consequences resulting from exposure to chemical insults of endogenous and exogenous origin. Even at equitoxic doses, different stressors induce distinctive and complex signaling cascades. The responses typically follow cell perturbations at the subcellular organelle level.
Expression of heme oxygenase 1 (HMOX1) is regulated by various indicators of cell stress. Cytoprotection by HMOX1 is exerted directly by HMOX1 and by the antioxidant metabolites it produces through the degradation of heme (Origassa et al, 2013; Ryter et al, 2006).
Reactive oxygen and nitrogen species (RONS) are important mediators of chemical stress, as they are produced endogenously in mitochondria, and also result from redox activities of many toxins and heavy metal cations. The points of RONS action in the cell are plasma and ER membrane lipids, as well as DNA, both acting as sensors for the cellular response. On the other hand, chemotherapeutic agents exert their action via generation of RONS and induction of cancer cell apoptosis, while drug resistance associates with RONS-induced cancer cell survival (Sampadi et al, 2020; Moldogazieva et al, 2018).