Cryptic losses under heat stress: oxidative stress-induced impairment of laying hen production performance and endogenous antioxidant interventions
发布时间：2026-06-15
From May to June 2026, South China and many parts of Southeast Asia will exhibit pronounced high-temperature and high-humidity conditions. In South China, temperatures began rising rapidly in late May, with persistent heat waves affecting numerous areas; additional heat events are expected throughout June. At the same time, above-average rainfall during the peak “Dragon Boat Rain” season will keep humidity elevated. The combination of heat and humidity creates a “steamer effect,” with apparent temperatures generally exceeding 35°C and at times surpassing 40°C. During the same period, Southeast Asia will also experience multiple heat waves, with maximum temperatures exceeding 40°C in many locations, and another two to three heat wave episodes anticipated in June. According to comprehensive meteorological model projections, there is an 85%–95% probability that the equatorial Pacific will transition into an El Niño state from June to September 2026, at which point both the frequency and intensity of heat waves in South China and Southeast Asia are expected to exceed long-term averages. These climatic characteristics imply that, from late May through the entire summer, livestock and poultry in the region will be subjected to prolonged exposure to hot, humid conditions, maintaining elevated risks of heat stress—an important external factor that can trigger oxidative stress in animals.
This sustained environmental stress is a key external factor that induces heat stress in livestock and poultry, subsequently triggering oxidative stress in the organism. High summer temperatures represent one of the most severe environmental challenges facing intensive livestock and poultry production. When ambient temperatures exceed the upper limit of the animals’ thermoneutral zone—generally 21–26°C for laying hens and 18–23°C for pigs—the animal body initiates a series of physiological compensatory responses, known as the heat stress response. Heat stress not only directly Receive guidance It leads to reduced feed intake and impaired production performance; more critically, it triggers profound metabolic disturbances within the body—oxidative stress. A large body of research indicates that heat stress is one of the primary environmental factors inducing oxidative stress in livestock and poultry, and Oxidative stress Precisely what causes The root cause of cellular dysfunction, tissue pathology, and reduced production performance.
Under heat stress, livestock and poultry increase their respiratory rate and peripheral blood flow to dissipate heat, while sympathetic nervous activity rises and metabolic rate increases. This process leads to increased electron leakage in the mitochondrial electron transport chain and a dramatic surge in reactive oxygen species (ROS), which can rise to levels up to 2-3 fold), while heat stress inhibits Nrf2 Nuclear translocation, resulting in SOD, GSH-Px When the expression of endogenous antioxidant enzymes is downregulated, ROS Excessive production and the suppression of antioxidant defenses create a vicious cycle, ultimately plunging the cell into a state of oxidative stress. It should be emphasized that, Oxidative stress is a root cause of heat stress injury. rather than one of the parallel mechanisms. Traditionally recognized factors such as respiratory alkalosis, electrolyte disturbances, and impaired intestinal barrier function are, at their core, downstream effects of oxidative stress: ROS attack ion pumps in cell membranes (e.g., Na⁺/K⁺-ATPase), disrupting ionic homeostasis; oxidative damage compromises tight junction proteins in the intestinal epithelium, leading to leaky gut; and energy depletion resulting from mitochondrial dysfunction further exacerbates systemic compensatory failure. In other words, without eliminating excess ROS at its source and restoring mitochondrial function, simply administering alkali, potassium, or modulating the gut microbiota is akin to “skimming the surface” without addressing the root cause. Only by activating the endogenous antioxidant system at its origin represents the key breakthrough for overcoming the challenges posed by heat stress.
Figure 1 Mechanism of oxidative stress induced by heat stress in poultry (Nima, 2021)
Oxidative stress initially targets mitochondria—the cell’s “powerhouses.” Mitochondrial membranes are rich in unsaturated fatty acids and highly susceptible to ROS. Lipid peroxidation leads to a decline in mitochondrial membrane potential and reduced ATP synthesis, plunging cellular energy metabolism into crisis. The clinical manifestations in animals with different production orientations are as follows:
Figure 2 Basic structure and function of mitochondria
Laying hens: Ovarian granulosa cells are a primary target of oxidative stress. Apoptosis or ferroptosis of granulosa cells accelerates follicular atresia and arrests follicular development, leading to reduced egg production. Oviduct mucosal cells suffer functional disruption due to oxidative damage, resulting in uneven calcium and matrix deposition in the shell gland and the formation of “watermark eggs,” cracked eggs, and thin-shelled eggs, thereby sharply decreasing the proportion of high‑quality eggs. Meanwhile, heat stress suppresses the synthesis of intestinal calcium‑binding proteins, further exacerbating shell quality problems.
Sow: Oxidative stress impairs oocyte maturation and embryo implantation, leading to increased return-to-estrus rates and reduced litter sizes. In the late stages of gestation, oxidative stress can trigger placental dysfunction, compromising fetal development.
Piglets and growing pigs: Oxidative stress disrupts tight junctions in the intestinal epithelium, increases intestinal permeability, and triggers diarrhea and endotoxin translocation into the bloodstream. At the same time, it inhibits protein synthesis, promotes muscle proteolysis, and reduces average daily gain and feed conversion ratio.
Direct impact on the economic performance of farms: In summer, laying hens typically experience a 5–10% drop in egg production, with the proportion of broken or cracked eggs rising by 10–20%, and the percentage of premium-grade eggs falling to 60–70%. Taking a farm with 100,000 hens as an example, losses from foregone premium‑egg premiums can amount to several hundred to over a thousand yuan per day, totaling hundreds of thousands of yuan over the entire summer. Heat stress in sows reduces conception rates by 10–15% and lowers farrowing rates, decreasing the number of weaned piglets per sow per year (PSY) by 1–2. At 400 yuan per weaned piglet, a sow herd of 10,000 could incur annual losses of 400,000–800,000 yuan. Growing-finishing pigs show a 5–15% decline in average daily gain, with feed conversion ratios worsening by 0.2–0.5, prolonging time to market and increasing feeding costs. Oxidative stress also weakens immune defenses, raising the risk of secondary infections and leading to higher mortality and medication expenses.
In the reproductive system of laying hens, Granulosa cells It is a key regulator of follicular development, oocyte maturation, and hormone synthesis. It supplies nutrients to the oocyte and maintains a stable follicular microenvironment. However, granulosa cells are highly sensitive to oxidative stress. Studies have shown that oxidative stress leads to a sharp increase in intracellular ROS levels, a decrease in mitochondrial membrane potential, and disruption of intracellular Ca²⁺ homeostasis, ultimately triggering apoptosis or ferroptosis. Once granulosa cells undergo extensive apoptosis, follicular atresia accelerates, egg production declines, and eggshell quality deteriorates. (Hu Youjun, Journal of Animal Nutrition, 2025) research Research shows ： In the oxidative stress model, granulosa cells’ Nrf2 The signaling pathway is inhibited, and antioxidant enzymes ( SOD, GSH-Px ) Activity decreases, MDA Levels increase. Protecting the integrity of granulosa cells is key to maintaining egg production rates and delaying the decline after peak production.
Figure 3 Oxidative stress leads to premature ovarian failure
Traditional anti-stress strategies often rely on exogenous antioxidants (such as vitamin C and vitamin E) to provide short-term protection by directly scavenging free radicals. However, these compounds are rapidly metabolized and easily oxidized and inactivated in the body, and they fail to activate the organism’s intrinsic endogenous antioxidant network. In contrast, Endogenous Antioxidation The core of the strategy lies in activating the body’s intrinsic antioxidant defense systems (such as the Nrf2-ARE signaling pathway) and upregulating the expression of endogenous antioxidant enzymes (SOD, CAT, GSH-Px, etc.), thereby achieving sustained, systemic regulation of oxidative stress (E Xiaodi, Chinese Journal of Animal Husbandry & Veterinary Medicine, 2024).
Based on their mechanisms of action, the antioxidants commonly used in production can be classified into the following four categories.
1. Direct free radical scavenging type
Representative substance: Vitamin C, vitamin E, carotenoids, etc.
Mechanism of action: By donating hydrogen atoms or single electrons, it directly quenches reactive oxygen species (ROS) and reactive nitrogen species (RNS), thereby interrupting the chain reaction of lipid peroxidation. Limitations: It is a consumable antioxidant with a short duration of action; at high doses, it may exert pro-oxidant effects.
Figure 4. Antioxidant mechanism of vitamin C (Azzi, 2019)
2. Antioxidant enzyme cofactor type
Representative substance: Selenium (Se), zinc (Zn), manganese (Mn), copper (Cu), etc.
Mechanism of action: As an essential cofactor or activator of the endogenous antioxidant enzymes GSH-Px, SOD, and CAT, it ensures the catalytic activity of these enzymes. Limitations: These substances merely supply the “building blocks” required for enzymatic activity and cannot upregulate the expression levels of antioxidant enzymes; excessive supplementation carries a risk of toxicity.
Figure 5 Mechanism of trace elements scavenging free radicals (Jan, 2012)
3. Signal Pathway Activator
Representative substance: Flavonoids (such as soy isoflavones, vine tea flavonoids, quercetin, and kaempferol), phenolic acids (such as resveratrol and curcumin), terpenoids, and others.
Mechanism of action: Activation of the Keap1-Nrf2-ARE signaling pathway. Under resting conditions, Nrf2 binds to Keap1 and is ubiquitinated for degradation. Flavonoids covalently modify key cysteine residues (Cys151, Cys273, Cys288) in the Keap1 protein, leading to the release of Nrf2, its translocation into the nucleus, and its heterodimerization with Maf proteins. This complex binds to ARE sequences and activates transcription of downstream genes, including SOD, CAT, GSH-Px, HO-1, NQO1, GST, and others. Advantages: A single activation sustains the expression of antioxidant proteins for hours to days, systemically enhancing defense networks without requiring high concentrations of exogenous intervention. Limitations: Onset of action is relatively slow (3–7 days), and bioavailability varies considerably.
Figure 6 Regulatory effects of flavonoids on antioxidant pathways
4. Other Supportive Antioxidant Strategies
Organic acidifiers (fumaric acid, citric acid): As an intermediate of the tricarboxylic acid cycle, it can supply substrates to mitochondria under energy-depleted conditions caused by heat stress, thereby promoting ATP synthesis and indirectly reducing ROS production.
Experiment 1: Jingfen No. 6 laying hens from 23 to 60 weeks of age
Add specific flavonoid antioxidants (Qimei Su) Subsequently, the egg-laying rate increased from 91.4% to 93.7%; serum T-AOC, SOD, and GSH-Px levels rose significantly, while MDA levels declined significantly; the feed-to-egg ratio decreased, and eggshell strength improved.
Experiment 2: A layer farm with 1 million hens (56,000 samples)
As shown in the figure below, during weeks 50–54, the average laying rate exceeded the standard by 1.64%. From weeks 55 to 60, compared with the Jingfen No. 6 standard, the laying rate steadily increased, averaging 4.64% above the standard. This study found that supplementing feed with Qimei Su during the late peak-laying period slowed the decline in laying rate and extended the duration of the peak phase; after five weeks, it significantly improved the laying rate of Jingfen No. 6 hens and reduced mortality and culling rates.
Experiment 3: Laying hens at 76 weeks of age in the late production phase
Compared with the control group, adding to the feed of laying hens at 76 weeks of age In the Qimei strain, the egg production rate increased from 77.81% to 80.17%, and the numbers of graded follicles and large white follicles increased significantly.
Addressing summer heat stress requires establishing a multi-faceted prevention and control system that integrates environmental management, nutritional regulation, and endogenous activation.
1. Environmental Management: Install water curtains and misting systems, and enhance ventilation; shift feeding to the cooler morning and evening hours; ensure an adequate supply of clean drinking water, which may be supplemented with sodium bicarbonate or potassium chloride.
2. Nutritional Regulation:
Energy: Adding fats to replace some carbohydrates reduces the thermic effect of food.
Protein: Appropriately reduce crude protein levels, balance essential amino acids (such as lysine and methionine), and decrease nitrogen excretion.
Electrolyte: Maintain dietary electrolyte balance (dEB value 200–250 mEq/kg) and supplement potassium, sodium, and bicarbonate.
Vitamins: Increase the inclusion levels of VC, VE, VA, and B vitamins; a recommended level of 200–400 g/ton of feed is suggested for VC.
Trace elements: Supplement with organic selenium, chromium, zinc, and manganese to enhance antioxidant enzyme activity.
Plant extracts: Flavonoids and polyphenolic compounds exhibit significant antioxidant and anti-inflammatory activities.
Activating the animal’s intrinsic endogenous antioxidant system is a crucial step.
Based on antioxidant mechanisms, Acid NIC has developed “Qimeisu,” an antioxidant with highly effective active ingredients, using molecular simulation techniques and formulation synthesis, along with specifically screened and structurally modified Lewis acids (daidzein). Its key features are:
Conclusion
Antioxidant protection is not an “optional choice” but a “must-answer question.”
Heat stress has become a common occurrence in summer aquaculture, with oxidative stress serving as the underlying root cause. Integrated prevention and control requires a holistic approach. Environmental Management, Nutritional Regulation, and Endogenous Activation The combined effect of these three factors is key. By scientifically applying endogenous antioxidant strategies to eliminate free radicals at their source and restore mitochondrial function, we can achieve the goal of “maintaining production under high temperatures without compromising performance.”
Please see the related links.
2. 《 Antioxidant Defense in Granulosa Cells: The Secret to Sustained High Production in Laying Hens? 》
5. 《 A Nutritional Plan for Keeping Laying Hens Young and Healthy: The “Three Goods” Approach 》
Written by: E Xiaodi
Reviewed by: Hu Youjun
Arranged by: Teng Jiahao
Keywords:
More News
Key point: Necrotic enteritis (NE) caused by Clostridium perfringens type A results in annual losses across
07-24
2026
This year, the “typical hot and sunny” conditions of the Indian summer are mainly concentrated along a band stretching from the middle and lower reaches of the Yangtze River through Jiangnan to Sichuan, Chongqing, and the Huang-Huai region. In South China, due to above-normal rainfall, abundant cloud cover, and moderating sea breezes, August temperatures…
09-04
2026
Research on the mechanisms and regulation of oxidative stress in animals has been one of the major research focuses in animal nutrition and livestock and poultry health over the past decade. The selection of various free radical scavengers and investigations into their mechanisms have attracted considerable scientific attention.
10-26
2024
Value-driven, with deep collaboration with customers
Laboratory Test Sharing
Collaborative R&D
Product Customization Services
Comprehensive Solution
acid Consultation Sharing
We're here to help!
Send us a message or discuss your needs with us, and you're sure to receive the right response.
Phone:
Email:
Address:
Guangqing Industrial Park, Shijiao Town, Qingcheng District, Qingyuan City, Guangdong Province
Guangqing Industrial Park, Shijiao Town, Qingcheng District, Qingyuan City, Guangdong Province
Guangqing Industrial Park, Shijiao Town, Qingcheng District, Qingyuan City, Guangdong Province
Guangqing Industrial Park, Shijiao Town, Qingcheng District, Qingyuan City, Guangdong Province
Copyright © Guangdong nuacid Biotechnology Co., Ltd.