Heat stress (HS) is one of the most important stressors in chickens, and its adverse effects are primarily caused by disturbing the redox homeostasis. An increase in electron leakage from the mitochondrial electron transport chain is the major source of free radical production under HS, which triggers other enzymatic systems to generate more radicals. As a defense mechanism, cells have enzymatic and non-enzymatic antioxidant systems that work cooperatively against free radicals. The generation of free radicals, particularly the reactive oxygen species (ROS) and reactive nitrogen species (RNS), under HS condition outweighs the cellular antioxidant capacity, resulting in oxidative damage to macromolecules, including lipids, carbohydrates, proteins, and DNA. Understanding these detrimental oxidative processes and protective defense mechanisms is important in developing mitigation strategies against HS. This review summarizes the current understanding of major oxidative and antioxidant systems and their molecular mechanisms in generating or neutralizing the ROS/RNS. Importantly, this review explores the potential mechanisms that lead to the development of oxidative stress in heat-stressed chickens, highlighting their unique behavioral and physiological responses against thermal stress. Further, we summarize the major findings associated with these oxidative and antioxidant mechanisms in chickens.

Reduced feed intake during heat stress (HS) disrupts glucose homeostasis, thereby resulting in endoplasmic reticulum (ER) stress and triggering apoptosis in chickens. We hypothesize that glucose supplementation could reduce apoptosis in chickens raised under HS. This study comprised 456 28-day-old broiler chickens randomly assigned to four treatment combinations under glucose supplementation and HS. The treatments were TN₀, TN₆, HS₀, and HS₆ with two glucose levels (0% and 6%) and two temperature levels (25 °C (thermoneutral-TN) and 35 °C (8.00 AM to 8.00 PM, (HS)). After 7 days post-HS, the blood glucose level for the HS₆ group was higher than for TN₀, TN₆, and HS₀. We studied the mRNA expression of genes and caspase-3 activity in the four experimental groups. The expressions of GCN2, ATF4, CHOP, and FOXO3a increased during HS regardless of glucose supplementation, while PERK and MAFbx increased only under HS with glucose supplementation. We show that under TN conditions, glucose supplementation led to a significant increase in cellular apoptosis in the Pectoralis (P.) major. However, under HS with glucose, the level of apoptosis was similar to that of chickens raised under TN conditions with no glucose supplementation. The utility of glucose to curtail apoptosis under HS should be tested under other intense models of HS.

Eimeria (E.) maxima invades the midgut of chickens and destroys the intestinal mucosa, impacting nutrient digestibility and absorption. Heat stress (HS) commonly affects the broiler chicken and contributes to inflammation and oxidative stress. We examined the independent and combined effects of HS and E. maxima infection on apparent amino acid ileal digestibility (AID) and mRNA expression of amino acid transporters in broiler chickens (Ross 708). There were four treatment groups: thermoneutral-control (TNc) and infected (TNi), heat-stress control (HSc) and infected (HSi), six replicates of 10 birds/treatment. Ileal content and tissue were sampled at 6 d post infection to determine AID and transporters expression. Surprisingly, the HSi chickens exposed to two critical stressors exhibited normal AID. Only the TNi group displayed reduction in AID. Using TNc as control, the HSc group showed upregulated CAT1, LAT4, TAT1, SNAT1, and SNAT7. The HSi group showed upregulated CAT1 and LAT1, and downregulated b^0,+AT, rBAT, SNAT1, and SNAT2. The TNi group showed upregulated CAT1, LAT1, and SNAT1 and downregulated B⁰AT1, b^0,+AT, rBAT, LAT4, and TAT1. The expression of all enterocytic-apical and about half of the basolateral transporters was higher in the HSi group than in the TNi group, indicating that HS can putatively alleviate the E. maxima adverse effect on ileal digestion and absorption.

Heat stress (HS) causes molecular dysfunction that adversely affects chicken performance and increases mortality. The responses of chickens to HS are extremely complex. Thus, the aim of this study was to evaluate the influence of acute and chronic exposure to HS on the expression of thioredoxin–peroxiredoxin system genes and DNA methylation in chickens. Chickens at 14 d of age were divided into two groups and reared under either constant normal temperature (25 °C) or high temperature (35 °C) in individual cages for 12 days. Five birds per group at one and 12 days post-HS were euthanized and livers were sampled for gene expression. The liver and Pectoralis major muscle were sampled for cellular analysis. mRNA expression of thioredoxin and peroxiredoxins (Prdx) 1, 3, and 4 in the liver were down-regulated at 12 days post-HS compared to controls. The liver activity of thioredoxin reductase (TXNRD) and levels of peroxiredoxin1 (Prdx1) at 12 days post-HS were significantly decreased. The results reveal that there was a significant decrease in DNA methylation at 12 days post HS in liver tissues. In conclusion, pathway of thioredoxin system under HS may provide clues to nutritional strategies to mitigate the effect of HS in meat-type chicken.

Molecular differences exist between birds with high residual water intake (HRWI) compared to those with low residual water intake (LRWI). Residual water intake (RWI) is defined as the difference between the water intake of a bird and the expected water intake corrected for metabolic body weight, feed intake, and body weight gain. Tissue metabolomic analysis revealed significantly increased kidney glucose, fructose, and arabitol in the LRWI group compared to the HRWI group. mRNA expression analysis of apical sodium glucose cotransporters SGLT1, SGLT4, SGLT5, and SGLT6 showed decreased expression of SGLTs 1, 5, and 6 in LRWI birds (p < 0.05), whereas SGLT4 expression was increased compared with HRWI birds (p < 0.01). An analysis of basal glucose transporters GLUT1, GLUT2, GLUT5, and GLUT9 showed significantly increased GLUT2 expression in LRWI birds compared with HRWI birds (p < 0.01). We postulate that SGLT4 is the main apical transporter in chicken kidneys and that its increased expression reduces these birds’ need for water, resulting in less drinking. This is balanced by the increased expression of the basal transporter GLUT2, indicating better glucose retention, which may partly explain the physiological mechanism behind why these birds drink less water. Innately driven broiler water intake could therefore be influenced by the expression of kidney solute transporters.