Environmental Contaminants and Redox Homeostasis

Contaminants in the environment, such as oxidant fuels, chemical substances, particulate surfaces, cigarette smoke, toxins, metals, medicines, xenobiotics, or radiation, can trigger the generation of the reactive oxygen species (ROS) or the reactive nitrogen species (RNS), which can lead to oxidative stress. Many ROS-mediated mechanisms shield cells from oxidative damage and help them reclaim their redox homeostasis. The activation of metabolic or bioenergetics reaction processes mediated by thiol redox switches is one of the overt or indirect mechanisms of oxidative stress. Furthermore, toxic agents' oxidative stress can be exacerbated through metabolic processes in cells. Excess ROS is regulated by endogenous antioxidant protection mechanisms (both enzymatic and non-enzymatic), which help remove toxic oxygen molecules or scavenge ROS under normal conditions. To sustain redox homeostasis in the presence of environmental stress, the cells are fitted with several complementing energy-dependent structures. The cytochrome (CYP) enzymes are a monooxygenase superfamily that includes several enzymes involved in xenobiotic detoxification. As a result, it seems that the CYP families are the most prominent members. Heavy metal toxicity, such as zinc, arsenic, and cadmium, is believed to be caused by their interaction with sulfhydryl groups in biological systems. Many sulfhydryl residues in antioxidant proteins, including metallothionein and albumin, serve as a sink for heavy metal ions, saving important protein thiols in the process.

Keywords: Antioxidants, Carotenoid, Drugs and Xenobiotics, Environmental Pollutants, GPx, GSH, Ionizing Radiations, Lipoic Acid, Metals, Pesticides, Reactive Oxygen Species, Redox Homeostasis, SOD, Tobacco Smoke, Vitamins.