Influence of Extracellular Protein on the Cytoprotective Effects of Two Model Phytochemicals
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Cell metabolism constantly produces reactive oxygen species (ROS) as a natural by-product of the normal metabolism of oxygen. This situation is not damaging because cells are able to compensate and maintain an adequate homeostasis between ROS production and its removal via enzymatic or non-enzymatic pathways. On the other hand, if this balance is disturbed by an excessive accumulation of ROS due to some reason related with environment, life style and pathologic factors these result in a situation called oxidative stress (OS). In consequence, this accumulation of ROS above the protection system of cells may damage the integrity and function of critical molecules, ultimately leading to cell death. There is increasing evidence that oxidative stress contributes to disease conditions such as cancer, chronic obstructive pulmonary disease, asthma, cardiovascular dysfunction and immunosuppression. Quercetin (Q) (2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-1- benzopyran-4-one; shown in Figure 1) is considered as one of the most abundant flavonoids and represents an integral part of human diet. High amounts of quercetin are found in numerous vegetables, fruits, nuts, tea, seeds and wine. It exhibits a wide range of biological activities, including anti-inflammatory anti-carcinogenic and antiviral actions. The chemoprevention elicited by polyphenols such as Q is mediated by apoptosis in tumor cells through direct activation of caspase cascade (mitochondrial pathway) such as caspase 3 and 9 as well as Bcl-2 family members but is without effect on their normal cell counterparts. Moreover, it exerts a notable cytoptotection activity against t-BHP-induced oxidative stress in HepG2 cells .