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In modern animal husbandry, stress can be viewed as an automatic response triggered by exposure to adverse environmental conditions. This response can range from mild discomfort to severe consequences, including mortality. The poultry industry, which significantly contributes to human nutrition, is not exempt from this issue. Although genetic selection has been employed for several decades to enhance production output, it has also resulted in poor stress resilience. Stress is manifested through a series of physiological reactions, such as the identification of the stressful stimulus, activation of the sympathetic nervous system and the adrenal medulla, and subsequent hormonal cascades. While brief periods of stress can be tolerated, prolonged exposure can have more severe consequences. For instance, extreme fluctuations in environmental temperature can lead to the accumulation of reactive oxygen species, impairment of reproductive performance, and reduced immunity. In addition, excessive noise in poultry slaughterhouses has been linked to altered bird behaviour and decreased production efficiency. Mechanical vibrations have also been shown to negatively impact the meat quality of broilers during transport as well as the egg quality and hatchability in hatcheries. Lastly, egg production is heavily influenced by light intensity and regimens, and inadequate light management can result in deficiencies, including visual anomalies, skeletal deformities, and circulatory problems. Although there is a growing body of evidence demonstrating the impact of environmental stressors on poultry physiology, there is a disproportionate representation of stressors in research. Recent studies have been focused on chronic heat stress, reflecting the current interest of the scientific community in climate change. Therefore, this review aims to highlight the major abiotic stressors in poultry production and elucidate their underlying mechanisms, addressing the need for a more comprehensive understanding of stress in diverse environmental contexts.
In modern animal husbandry, stress can be viewed as an automatic response triggered by exposure to adverse environmental conditions. This response can range from mild discomfort to severe consequences, including mortality. The poultry industry, which significantly contributes to human nutrition, is not exempt from this issue. Although genetic selection has been employed for several decades to enhance production output, it has also resulted in poor stress resilience. Stress is manifested through a series of physiological reactions, such as the identification of the stressful stimulus, activation of the sympathetic nervous system and the adrenal medulla, and subsequent hormonal cascades. While brief periods of stress can be tolerated, prolonged exposure can have more severe consequences. For instance, extreme fluctuations in environmental temperature can lead to the accumulation of reactive oxygen species, impairment of reproductive performance, and reduced immunity. In addition, excessive noise in poultry slaughterhouses has been linked to altered bird behaviour and decreased production efficiency. Mechanical vibrations have also been shown to negatively impact the meat quality of broilers during transport as well as the egg quality and hatchability in hatcheries. Lastly, egg production is heavily influenced by light intensity and regimens, and inadequate light management can result in deficiencies, including visual anomalies, skeletal deformities, and circulatory problems. Although there is a growing body of evidence demonstrating the impact of environmental stressors on poultry physiology, there is a disproportionate representation of stressors in research. Recent studies have been focused on chronic heat stress, reflecting the current interest of the scientific community in climate change. Therefore, this review aims to highlight the major abiotic stressors in poultry production and elucidate their underlying mechanisms, addressing the need for a more comprehensive understanding of stress in diverse environmental contexts.
This study investigated the effect of neonatal α-ketoglutaric acid (AKG) gavage feeding on broilers. The first experiment was conducted to determine the effect of AKG on day-old broilers. A total of seventy-two-day-old Ross 308 broiler chicks were divided into four treatment groups: (i) Two groups of chicks with gavage feeding of 0.6 mL of distilled water (DDW) for four consecutive days (CON); (ii) chicks fed with 0.6 mL of 0.1% AKG dissolved in DDW on the day of hatch (AL) followed by 0.2%, 0.3%, and 0.4% for three consecutive days; and (iii) chicks fed with 0.6 mL of 0.2% AKG dissolved in DDW on the day of hatch (AH) followed by 0.4%, 0.6%, and 0.8% for three consecutive days. Twenty-four hours after the first gavage feeding, six birds per treatment were slaughtered to study the organ development. Chicks fed with AKG showed higher absolute (p = 0.015) and relative (p = 0.037) weights of the gizzard. The AH group had higher absolute (p = 0.012) and relative (p = 0.035) heart weights. The second experiment was carried out to determine the effect of AKG on 15-day-old broilers under acute heat stress (AHS) for 3.5 h at 33 ± 1 °C. Forty-eight birds (12 per treatment) were raised until 15 days of age, divided into four treatments with equal numbers (n = 12), and given one of the following four treatments: (i) CON group reared at standard temperature (25 ± 1 °C) (CON-NT); (ii) CON group subjected to AHS (33 ± 1 °C) for 3.5 h (CON-HT); (iii) AL group subjected to AHS (33 ± 1 °C) for 3.5 h (AL-HT); and (iv) AH group subjected to AHS (33 ± 1 °C) for 3.5 h (AH-HT). There was a significant reduction in the change in BW (ΔBW, p = 0.005), an increase in the final rectal temperature (RTf) (p = 0.001), and a decreased final body weight (BWf) for all the treatments under AHS. Further, AHS led to an increased expression of hepatic heat shock protein (HSP)70 (p = 0.009), nicotinamide adenine dinucleotide phosphate hydrogen oxidase (NOX)1 (p = 0.006), and NOX4 (p = 0.001), while nuclear factor erythroid 2-related factor (NRF2), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase 1 (GPX1) remained significantly unaffected. Hepatic expression of HSP90 decreased in the AL-HT treatment as compared to CON-HT (p = 0.008). Plasma antioxidant status measured by malondialdehyde (MDA) concentration and antioxidant balance (AB) improved linearly (p = 0.001) as the concentration of AKG increased. Neonatal gavage feeding of AKG could potentially alleviate heat stress in broilers by enhancing plasma antioxidant levels and modulating HSP90 expression in the liver.
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