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The antioxidant defence mechanisms in the human/animal body are based on several options: decrease localized oxygen concentration; decrease activity of pro-oxidant enzymes and improve efficiency of electron chain in the mitochondria decreasing superoxide production; redox-signalling with induction of various transcription factors (e.g. Nrf2 and NF-kB) and gene expression with antioxidant response element-related synthesis of antioxidant enzymes (superoxide dismutase, glutathione (GSH) peroxidase, catalase, GSH reductase, GSH transferase, etc.) and other important protective molecules; vitagene activation and increased expression of protective molecules (heat shock protein, thioredoxins, sirtuins, superoxide dismutase, etc.); binding metal ions and metal chelating; decomposition of peroxides by converting them to non-radical, nontoxic products; chain breaking by scavenging intermediate radicals such as peroxyl and alkoxyl radicals; antioxidant recycling mechanisms; repair and removal of damaged molecules; apoptosis activation: to remove terminally damaged cells and restrict mutagenesis. It seems likely that development of the vitagene network concept is a new direction in explaining molecular mechanisms of stresses and for development of the effective strategies to prevent detrimental consequences of stresses.