Vitamin e supplementation enhances lipid oxidative stability via increasing vitamin e retention, rather than gene expression of mapk-nrf2 signaling pathway in muscles of broilers

Abstract

Dietary vitamin E (VE) supplementation is a method to produce VE-enriched meat and improve meat lipid oxidative stability. We aimed to study the effect of the VE supplementation duration on meat lipid oxidative stability, VE retention, and antioxidant enzymes’ activity, and explore its relationship with the mitogen-activated protein kinases (MAPK)-nuclear factor-erythroid 2-related factor 2 (Nrf2) signaling pathway in broilers slaughtered after electrical stunning. A total of 240 male 18-day-old Arbor Acres Plus broilers were distributed to four treatments, with six replicates in each treatment, and ten broilers per replicate. Broilers were fed with a basal diet (no supplementation of VE) or VE diet (200 IU/kg VE, DL-α-tocopherol) for one (W1), two (W2), or three (W3) weeks before electrical stunning (130 mA, 60 Hz, for 1s) and slaughter. The VE retention was positively and linearly affected (p < 0.01) by the VE feeding duration at one to three weeks before slaughter, and negatively (all p < 0.01) related to the thiobarbituric acid reactive substance (TBARS) content in both breast and thigh muscles at d 0, d 2, and d 6 postmortem. The VE retention was negatively (p < 0.05) related to the gene expression of c-Jun N-terminal kinases 1 (JNK1) and 2 (JNK2), Nrf2 in breast muscles, and JNK1 and p38 MAPK in thigh muscles. In conclusion, dietary vitamin E supplementation at 200 IU/kg for three weeks before electrical stunning and slaughter improved lipid oxidative stability via increasing VE retention, rather than the regulation by gene expression of the MAPK-Nrf2 signaling pathway in skeletal muscles of broilers.