Oxidative Stress Reactive species, including free radicals, reactive oxygenspecies, and reactive nitrogen species, are producedas a result of normal physiological processes and play importantroles in cellular signalling, gene transcription,and the immune response [1] . In the process of aerobicmetabolism, electron leakage along the electron transportchain in the mitochondria results in the productionof the superoxide anion (O 2– ). Other biological reactions,including oxidative bursts produced by phagocytes andenzyme systems such as cytochrome P450 and xanthineoxidase, also contribute to the production of these highlyreactive species [2] . Excessive production or accumulationof reactive species, however, can have detrimentaleffects by participating in reduction-oxidation (redox)reactions causing damage tomacromolecules, cell membranesand DNA [1, 3] . Thiscan alter biological propertiesof membranes, enzymes andreceptors, impair cell functioning,and lead to cell death [4] . For this reason, a complexnetwork of defense systems has developed in humans to protect against excessiveproduction of and damage by reactive species in an effortto maintain ‘redox homeostasis’ [1] . When the productionor accumulation of free radicals or reactive oxygenand nitrogen species surpasses the body’s ability to defendthem, a state of oxidative stress (or nitrosative stress)results [1, 4] . In addition to direct damage to biologicalmolecules and tissues, oxidative stress can also activatetranscription factors such as nuclear factor B (NF- B),which trigger signalling cascades resulting in cytokinerelease and inflammation [5]
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