ISSUE FOCUS 30 FEED & ADDITIVE MAGAZINE July 2023 OUTCOMES OF HEAT STRESS Oxidative stress Oxidative stress, simply put, occurs when the amount of reactive oxygen species (ROS) and nitrogen reactive species (NRS), exceed the antioxidant capacity of the cells. 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. The normal metabolism of the animal – its energy production – generates ROS and RNS, such as hydroxyl radicals, superoxide anions, hydrogen peroxide, and nitric oxide. These usually are further processed by antioxidant enzymes produced by the cell, 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. When the generation of ROS exceeds the capacity of the antioxidant system, oxidative stress ensues. Heat stress leads to higher cellular energy demand, promoting an overload of ROS in the mitochondria. Consequently, oxidative stress occurs in several tissues, leading to cell apoptosis or necrosis as oxidized molecules can take electrons from other molecules, resulting in a chain reaction. Among these tissues, the gastrointestinal tract can be highly affected. Impaired gut function In the gastrointestinal tract, oxidative stress and the consequent tissue damage, lower feed digestion and absorption, increase intestinal permeability and modify the microbiome. Changes in intestinal morphology and digestive function Heat stress affects intestinal weight, length, barrier function, and microbiota, resulting in animals that have lower total and relative weight of the small intestine, with shorter jejunum and duodenum, shorter villi (Figure 2), and reduced absorption areas, in comparison to non-stressed animals. Changes in the intestinal microbiome Due to reduced feed intake and impaired intestinal function, the presence and activity of the commensal microbiota can also be modified. Heat stress can lead to reduced populations of beneficial microbes, boost the growth of potential pathogens leading to dysbiosis and necrotic enteritis. Changes in intestinal permeability Several studies indicate that both acute and chronic heat stress increase gut permeability, not only by lowering feed intake, but also by increasing intestinal oxidative stress and disrupting the expression of tight junction proteins. Heat and oxidative stress in the gut result in cell injury and apoptosis. When the tight junction barrier is compromised, luminal substances leak into the bloodstream, which constitutes the condition known as “leaky gut”. This includes the translocation of pathogenic bacteria, including zoonotic pathogens (e.g. Salmonella and Campylobacter); consequently, a higher risk of contamination of food products can be expected. Figure 2. Villous height and width of broilers exposed to heat stress in relation with the control group (100%). Villous height is always shorter than the control group, but width can increase as the organisms shows resilience to the stressful situations and aims to recover intestinal surface. (Adapted from Jahejo et al., 2016; Santos et al., 2019; Wu et al., 2018; Abdelqader et al., 2016 ; Santos et al., 2015 and Awad et al., 2018 – by order of appearance in the graph from left to right)
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