ISSUE FOCUS 60 FEED & ADDITIVE MAGAZINE July 2025 Vit. E&C GPx SOD CAT Decrease production of free radicals Scavenge and decompose free radicals Activate Nrf2 and vitagenes Thermal and oxidative stress Activate the molecular repair system Induce Apoptosis Remove damaged cells +++ GPx SOD CAT HSPs Msr PHGPx OXIDATIVE STRESS – A CONSEQUENCE OF HEAT STRESS Oxidative stress, simply put, occurs when the amount of reactive oxygen species (ROS – such as superoxide anions, hydrogen peroxide, and hydroxyl radicals) exceeds the antioxidant capacity of the cells.6, 14, 15 Oxidative stress is regarded as one of the most critical stressors in poultry production as it is a response to diverse challenges affecting the animals.2, 17 At a cellular level, the metabolism of the animal – its energy production – generates ROS and reactive nitrogen species (RNS), such as hydroxyl radicals, superoxide anions, hydrogen peroxide, and nitric oxide. These usually are further processed by antioxidant enzymes produced by the cell2, 15, including superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). Nutrients such as selenium and vitamins E, C, and A also participate in antioxidant processes.2, 5 When the generation of ROS exceeds the capacity of the antioxidant system, oxidative stress ensues.2, 16 Heat stress in poultry leads to higher cellular energy demand, promoting the generation of ROS in the mitochondria13, which exceed the antioxidant capacity of the organism. As a consequence, oxidative stress occurs in several tissues, leading to cell apoptosis or necrosis.11 Among these tissues, the gastrointestinal tract can be highly affected. Oxidative stress damages cell proteins, lipids, and DNA, and reduces energy generation efficacy.6 Moreover, oxidized molecules can take electrons from other molecules, resulting in a chain reaction. If not controlled, this reaction can cause extensive tissue damage.16 In response to oxidative stress, all antioxidants in the organism work together to re-establish homeostasis. Several steps in the oxidative stress response have been identified. Whether they take place depends on the intensity of the stressor, with ROS and RNS acting as signalling molecules. These steps include the internal synthesis of antioxidants, the activation of transcription factors or vitagenes, and the production of protective molecules (Figure 2). Figure 2. Summary of the antioxidant response First, decrease free radical production by decreasing oxygen availability and reducing the activities of enzymes responsible for ROS production (NADPH oxidase). Second, scavenge and decompose free radicals through natural antioxidants (vitamins E & C, GSH, SOD, GPx, and CAT). Third, activate Nrf2 and vitagenes to further stimulate the synthesis of antioxidants. Fourth, activate enzymatic systems responsible for damaged molecule repair (HSP, Msr, DNA-repair enzymes) and removal (PH–GPx). Fifth, induce apoptosis and other processes to deal with terminally damaged cells. (Adapted from Surai et al., 2019)
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