Abstract
The purpose of this study was to evaluate the effects of chitosan oligosaccharides (COS) on acute heat stress (AHS) induced poor meat quality by alleviating oxidative damage through mitogen-activated protein kinase-nuclear factor-erythroid 2-related factor 2-antioxidant responsive element (MAPK-Nrf2-ARE) signaling pathway. A total of 108 thirty-five-day-old Chinese indigenous broilers (Luhua chicken) was used for this 42-d experiment. The broilers were randomly allocated to 3 treatments: control group (CON), AHS group, and AHS with 400 mg/kg COS supplementation (AHS-C) group. Both CON and AHS groups given the basal diet, and the AHS-C group given the basal diet with 400 mg/kg COS supplementation. On d 42, broilers in the AHS and AHS-C groups treated with AHS (increasing temperature from 24 to 34°C in 2-h and held for another 2-h), and the CON group under normal temperature (24°C). AHS exposure elevated (P < 0.05) body temperature (rectal, comb, eyelids, and feet) of broilers, increased (P < 0.05) breast muscle lightness (L*), drip loss, share force, hydrogen peroxide (H(2)O(2)) scavenging activity, reactive oxygen species (ROS) production, malondialdehyde (MDA) content, and catalase (CAT) activity, however, decreased (P < 0.05) pH(45min), pH(24h), redness (a*), and relative expression of heme oxygenase-1 (HO-1). Compared to the AHS group, dietary COS supplementation increased (P < 0.05) breast muscle pH(45min), pH(24h), and a*, H(2)O(2) scavenging activity, as well as relative expression of HO-1 and glutathione peroxidase (GSH-Px), however, decreased (P < 0.05) drip loss, share force, superoxide anion free radicals (O(2)(•-)) scavenging activity, ROS production, and MDA content. It was concluded that AHS impaired meat quality, which may be related to oxidative damage, as evidenced by increasing ROS production, MDA content, and decreasing the relative expression of HO-1. Dietary COS supplementation could effectively elevate the meat quality of broilers exposed to AHS via decreasing ROS production, activating the Nrf2 pathway, and Nrf2-mediated HO-1 and GSH-Px gene expression.