Extensive research work done during last three decades gives a detailed account of the oxidative stress, a condition where oxidants, within the body, outnumber endogenous antioxidants or the latter’s level is, somehow, depleted in order to allow the oxidants to freely damage cells and tissues. This condition is reported to cause or lead to development of a variety of diseases including cardiovascular diseases (CVDs), neurological disorders, lung diseases, cancer and many more. There are so many published reports indicating an axial role of oxidants in the development of diseases. However, oxidative stress condition does not emerge spontaneously, rather it needs a stimulus to create destructive endogenous environment where oxidants prevail over the normal physiology. Body, itself, monitors and assures a perfect balance between oxidants and antioxidants. In order to induce an imbalance, a stimulus needs to assist in and increase the generation of free radicals within the body and/or suppress the expression or activities of endogenous antioxidants. Such kind of stimulus may include any of the physical, chemical or biological agents, normally categorised as ‘toxicants’ or ‘xenobiotics’. (Note: for most of the xenobiotics a particular mechanism of action is reported that is involved in induction of a specific condition, e.g. consumption of ethanol, carbontetrachloride (CCl4) or paracetamol (Acetaminophen) primarily induces hepatotoxicity; Cigarette smoke, automobile exhaust or suspended particulate matter (SPM) commonly induce lung toxicity. However, oxidative stress is reported to remain a common and integral part of the whole damaging mechanism).
Two points apparently becomes clear that (i) oxidative stress is not spontaneous, and (ii) it needs some stimulus to reach up to the level of causing oxidative damages. But the phenomenon is not so much simple as it appears through these two points. To understand the complexity of the event one needs to understand the very nature of the oxidants, which are mainly free radicals generated by essential physiological processes, the ways of their generations and the mechanism behind the macromolecular damages to the cells. The one also needs to understand the physico-chemical properties of the xenobiotics.
While going through the literature an ambiguity arises whether its oxidative stress which is an interface between xenobiotics exposure and the consequent toxicities or xenobiotics itself causes the toxicity and the oxidative stress condition arise as an effect. However, various recent published reports indicates that exposure to certain chemicals and consequent injuries is not just a matter of oxidant-antioxidant imbalance and it goes beyond that notion with an alteration in genetic material and gene expression, enzyme inhibition and ultimately affecting the normal physiology. But at the very same time oxidative stress arise and appear to play a crucial role in the development of toxicities. These two separately defined events are interwoven in such a way that it’s not easy to conclude whether the effect includes toxicities and oxidative stress or the cause includes chemical exposure and the oxidative stress. Oxidative stress seems at either side creating a mystery that continues.
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