Heat stress impairs mitochondria functions and induces oxidative injury in broiler chickens1

Huang, Chen; Jiao, Hongchao; Song, Zhigang; Zhao, Jingpeng; Wang, X.; Lin, Hai

doi:10.2527/jas.2014-8739

Cited by 168 publications

(113 citation statements)

References 55 publications

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“…Furthermore, heat exposure increased SOD and catalase activities in breast muscle but the reverse was true in thigh muscle. On the other hand, heat stress increased SOD and decreased GSH-Px activities of mitochondria regardless of muscle types [120]. Interestingly, in restrictedly fed broiler breeder's plasma MDA, protein carbonyl content, activity of SOD and corticosterone content were not altered after acute (33°C) and prolonged heat challenges [121].…”

Section: Heat Stressmentioning

confidence: 82%

Antioxidant Systems in Poultry Biology: Superoxide Dismutase

Surai¹

2016

J Anim Res Nutr

168

135

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Commercial poultry production is associated with various stresses responsible for decreasing productive and reproductive performance of growing chicks, breeders and commercial layers. A growing body of evidence shows that most of stresses in poultry production at the cellular level are associated with oxidative stress. Recently, a concept of the cellular antioxidant defense has been revised with special attention paid to cellular redox status maintenance and cell signaling. In fact, antioxidant systems of the living cell are based on three major levels of defense and superoxide dismutase (SOD) is shown to belong to the first level of the antioxidant defense network. Cellular antioxidant defenses are shown to include several options and vitagene activation in stress conditions is considered as a fundamental adaptive mechanism. The vitagene family includes various genes regulating synthesis of protective molecules including thioredoxins, sirtuins, heat shock proteins and SOD. However, by the time of writing no comprehensive review on the roles and effects of SOD in poultry biology has appeared. Therefore, the aim of this review is a critical analysis of the role of SOD in poultry biology with specific emphasis to its functions as an essential part of the vitagene network. From the analysis of the recent data related to SOD in poultry physiology and adaptation to stresses it is possible to conclude that: a) SOD as important vitagene is the main driving force in cell/body adaptation to various stress conditions. Indeed, in stress conditions additional synthesis of SOD is an adaptive mechanism to decrease ROS formation; b) If the stress is too high SOD activity is decreased and apoptosis is activated; c) there are tissue-specific differences in SOD expression which also depends on the strength of such stress-factors as heat, heavy metals, mycotoxins and other stressors; d) SOD is shown to provide an effective protection against lipid peroxidation in chicken embryonic tissues and semen; e) SOD is shown to be protective in heat and cold stress, toxicity stress as well as in other oxidative-stress related conditions in poultry production; f) there are complex interactions inside the antioxidant network of the cell/body to ensure an effective maintenance of homeostasis in stress conditions. Indeed, in many cases, nutritional antioxidants (vitamin E, selenium, carotenoids, phytochemicals, etc.) in the feed can increase SOD expression; g) nutritional means of SOD upregulation in stress conditions of poultry production and physiological and commercial consequences await further investigation; h) vitagene upregulation in stress conditions is emerging as an effective means for stress management.

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Section: Heat Stressmentioning

confidence: 82%

Antioxidant Systems in Poultry Biology: Superoxide Dismutase

Surai¹

2016

J Anim Res Nutr

168

135

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“…In humans, long-term corticosteroid administration increases 8-OHdG concentrations in association with mitochondrial DNA damage in skeletal muscles [51]. In our previous study, heat exposure-induced oxidative stress caused an increase in mitochondrial 8-OHdG in the breast and thigh muscles [15]. These results suggest that DEX induced oxidative damage in skeletal muscle mitochondria.…”

Section: Mitochondrial Dysfunction Is Associated With Increased Oxidamentioning

confidence: 76%

“…In DEXchickens, urate concentration (+14.4%) increased simultaneously with allantoin concentration (+103.3%), which is the end product of urate oxidation, indicating that urate was involved in the DEX-induced oxidative response [15]. However, urate can serve not only as an antioxidant but also as a pro-oxidant [39,40].…”

Section: Dex Induced Oxidative Damage In Plasmamentioning

confidence: 99%

“…All kits used in the present study have been successfully used in previous poultry studies [8,25]. Allantoin levels were measured via high-performance liquid chromatography (SPD-10AVP; Shimadzu, Kyoto, Japan) using a modification of the method of Grootveld and Halliwell [26], as described by Huang et al [15].…”

Section: Plasma Variable Measurementsmentioning

confidence: 99%

“…Mitochondria are the primary sites of ROS production [12][13][14]. During heat stress, impaired mitochondrial function in skeletal muscles induces oxidative damage in the skeletal muscles of broilers [15,16]. However, the influence of GCs on mitochondrial function in skeletal muscles and the resulting effects on the redox balance remain to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

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A high-caloric diet rich in soy oil alleviates oxidative damage of skeletal muscles induced by dexamethasone in chickens

et al. 2017

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A high-caloric diet rich in soy oil alleviates oxidative damage of skeletal muscles induced by dexamethasone in chickens, Redox Report, 23:1, 68-82, DOI: 10.1080/13510002.2017 Objective: Glucocorticoids (GCs) can induce oxidative damage in skeletal muscles. The purpose of this study was to demonstrate a high caloric (HC) diet rich in soy oil would change the oxidative stress induced by a GC. Methods: The effect of dexamethasone (DEX) and HC diet on oxidative stress in plasma, skeletal muscles (M. pectoralis major, PM; M. biceps femoris, BF), and mitochondria were determined. The biomarkers of oxidative damage and antioxidative enzyme activity were determined. The fatty acid profile of muscles and the activities of complex I and II in mitochondria were measured. Results:The results showed that DEX increased the concentrations of oxidative damage markers in plasma, muscles, and mitochondria. The activity of complex I was significantly suppressed by DEX. DEX-chickens had higher proportions of polyunsaturated fatty acids and lower proportions of monounsaturated fatty acids in the PM. A HC diet decreased the levels of oxidative damage biomarkers in plasma, muscles, and mitochondria. The interaction between DEX and diet suppressed the activities of complex I and II in HC-chickens. Discussion: Oxidative damage in skeletal muscles and mitochondria was the result of GC-induced suppression of the activity of mitochondrial complex I. A HC diet improved the antioxidative capacity and reduced the oxidative damage induced by the GC.

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