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The objective of this study was to explore the linkage of oxidative stress occurring in mitochondria, skeletal muscles, and plasma in heat stress-challenged broilers. At d 35, 24 broilers were randomly assigned to 2 treatments: rearing at high temperature (32 ± 1°C; heat stress group) or normal temperature (21 ± 1.2°C; control) for 7 d. The oxidative damage of lipid, DNA, and protein and the activities of antioxidative enzymes were measured, respectively, in plasma, skeletal muscles (breast and thigh muscles), and skeletal muscle mitochondria. The result showed that heat exposure increased (P < 0.01) plasma concentrations of thiobarbituric acid reacting substances (TBARS) and 8-hydroxydeoxyguanosine (8-OHdG) whereas it deceased total antioxidant capacity (P < 0.05) and ability to inhibit hydroxyl radicals (AIHR; P< 0.001). Protein carbonyl and TBARS levels were increased (P < 0.001) by heat stress in breast and thigh muscles. In skeletal muscle mitochondria, heat stress increased (P < 0.05) 8-OHdG and suppressed AIHR. Plasma activity of superoxide dismutase (SOD) was increased (P< 0.001) whereas glutathione peroxidase (GSH-Px) was suppressed by heat stress (P < 0.001). Heat exposure increased SOD and catalase activities in breast muscle (P < 0.01) but the reverse was true in thigh muscle (P < 0.05). Glutathione peroxidase was increased in thigh muscle (P < 0.001) but was not changed in breast muscle (P > 0.05). Heat stress increased SOD (P < 0.05) and decreased GSH-Px activities (P < 0.05) of mitochondria regardless of muscle types. Plasma allantoin level increased (P < 0.01) correspondingly with urate (P < 0.001) in heat-stressed broilers, indicating that urate could serve as an antioxidant to enhance the antioxidative capacity during stress in a concentration-dependent manner. The activities of respiratory chain complexes I and III were estimated in skeletal muscle mitochondria. Mitochondrial complex I activity was suppressed (P < 0.01) by heat exposure in breast and thigh muscles but complex III activity was elevated only in breast muscle (P < 0.01) of heat-stressed broiler. The fatty acid composition in skeletal muscle was not influenced by heat stress. In conclusion, suppressed mitochondrial complex I activity is associated with oxidative stress induced by heat exposure, which, in turn, is linked with the oxidative damages in muscle tissues and plasma.

In the present study, the effects of long-term exogenous glucocorticoids administration and dietary supplementation of alpha-tocopheryl acetate on the induction of lipid peroxidation in skeletal muscle were investigated. Male broiler chicks were randomly assigned to 2 diet treatments: the basal diet supplemented with 20 (low level of vitamin E) or 200 (high level of vitamin E) mg of vitamin E (as DL-alpha-tocopheryl acetate)/kg of diet. At 35 d of age, the chickens in each dietary treatment were randomly divided into 3 groups of 30 chickens and subjected to the following treatments: daily s.c. injection of dexamethasone (DEX, 2 mg/kg of BW) for 6 d, sham injection of saline (control), or the sham-treated pair-fed control that maintained the same feed intake as DEX treatment (pair-control). The results showed that the growth of chickens was suppressed by DEX, whereas it was improved by the high level of vitamin E treatment. The DEX treatment resulted in augmented plasma concentrations of TBA reacting substances. Muscle TBA reacting substances levels were higher in DEX chickens at both 24- and 48-h time points postslaughter. Vitamin E supplementation suppressed the formation of lipid peroxidation in both plasma and skeletal muscle tissues. Muscle activity of superoxide dismutase was significantly increased by DEX treatment in both musculus pectoralis major and musculus biceps femoris and maintained as such during the initial 48 h postmortem. The result of the present study indicated that DEX treatment increased the saturation level of skeletal muscle fatty acids. These results suggest that vitamin E supplementation was favorable for the performance of broiler chickens by alleviating the oxidative stress induced by DEX treatment.

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The effects of stocking density, sex, and dietary ME concentration on live performance, footpad burns, and leg weakness of broilers were investigated. A total of 876 male and 1,020 female 1-d-old chicks were placed in 24 pens to simulate final stocking density treatments of 26 kg (LSD; 10 males or 12 females/m(2)) and 42 kg (HSD; 16 males or 18 females/m(2)) of BW/m(2) floor space. Two series of experimental diets with a 150 kcal/kg difference in ME concentration (2,800, 2,900, and 3,000 or 2,950, 3,050, and 3,150 kcal of ME/kg) were compared in a 3-phase feeding program. The HSD treatment significantly decreased BW gain and feed conversion ratio (FCR). The HSD chickens consumed less feed by 35 d of age; thereafter, the reverse was true. Male chickens had significantly higher feed intake (FI), BW gain, and FCR compared with females. A significant interaction was found of stocking density and age for FI, BW gain, and FCR. Compared with LSD treatment, HSD broilers had a higher FI and a lower FCR from 36 to 42 d of age. Stocking density, sex, and age had a significant interaction for BW gain and FCR. Female broilers had worse BW gain and FCR when stocked at high density from 36 to 42 d of age. Stocking density had no significant influence on breast, thigh, or abdominal fat yield. Female broilers had significantly higher breast yield and abdominal fat. Male broilers and HSD treatment had high footpad burn and gait scores. A low ME diet increased footpad burn score but had no effect on gait score. The result indicated that stocking density had a more severe effect on the growth of male broilers before 35 d of age. Female broilers need more space than males at similar BW per square meter near marketing age. The incidence and severity of leg weakness are associated with sex, diet, and stocking density. This result suggests that the deteriorated effect of high stocking density is sex and age dependent.

1. Two experiments were conducted to investigate the effects of exogenous corticosterone administration (30 mg/kg diet) and dietary energy level on feed or energy intake and fat deposition in broiler chickens of 1 and 4 weeks of age. 2. Corticosterone treatment significantly suppressed body weight (BW) gain and reduced feed and caloric efficiencies. The retarded growth may conceal the stimulatory effect of corticosterone on feed consumption or metabolisable energy (ME) intake. A high-energy diet may increase energy intake and partially alleviate the suppressing effect of corticosterone on growth of broilers. 3. Corticosterone administration promoted the conservation of energy stores as fat at both abdominal and subcutaneous sites and this process occurred regardless of dietary energy level in ad libitum feeding status. A high-energy diet increased fat accumulation and showed no significant interaction with corticosterone treatment. 4. The suppressed development of breast and thigh muscles by corticosterone treatment was observed only in 1-week-old chickens fed on the low-energy diet. In contrast, the yield of breast muscle but not thigh muscle was significantly decreased by corticosterone in 4-week-old chickens, suggesting that the tissue specificity to corticosterone challenge is age dependent. 5. Plasma concentrations of glucose, insulin, triglyceride, non-esterified fatty acids (NEFA) and very low density lipoprotein were increased by corticosterone treatment regardless of diet treatment. A high-energy diet increased plasma levels of NEFA and resulted in hyperinsulinism in 4-week-old chickens but not in 1-week-old chickens. 6. Lipoprotein lipase (LPL) activities in adipose tissues may have been up-regulated by corticosterone treatment and showed tissue specificity. The increased LPL activities at ad libitum feeding status were not necessarily linked with the increased fat accumulation in corticosterone challenged chickens. 7. Corticosterone resulted in augmented energy consumption and altered energy redistribution toward lipid deposition. The induced insulin resistance and enhanced hepatic de novo lipogenesis by corticosterone are likely to be responsible for the increased fat deposition.