文摘
The present study investigated the effects of dietary trace mineral (Cu, Fe, Mn, and Zn) supplemental strategies on liver oxidative stress, endoplasmic reticulum stress, inflammation, and apoptosis of pigs. A total of 96 Duroc × Landrace × Yorkshire (DLY) piglets were randomly divided into four groups: considered or not considered the trace mineral concentrations in basal diet, and then added to the requirements proposed by NRC (2012) (+B/NR or −B/NR); and considered or not considered the basal diet’s trace mineral concentrations and then added to the level of commercial trace mineral supplement (+B/PL or −B/PL). Pigs were fed from 6.5 to 115 kg. Compared with +B/NR diets, −B/PL diets increased serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) concentrations (P < 0.05), resulted in high levels of Fe, Cu, Mn, and Zn accumulation in liver (P < 0.05), as well as led to hepatic oxidative damage with the high concentrations of thiobarbituric acid reactive substance (TBARS), protein carbonylation (PCO), and 8-hydroxyguanine (8-OHG) in liver (P < 0.05). Furthermore, pigs fed −B/PL diets increased CCAAT/enhancer-binding protein homologous protein (CHOP), eukaryotic initiation factor-2α (eIF-2a), interleukin-6(IL-6), B-cell lymphoma leukemia-2-associated X protein (Bax), and caspase-3, caspase-8, and caspase-9 gene expression (P < 0.05) in liver. −B/PL diets also up-regulated hepatic mRNA expression of phosphoenolpyruvate carboxykinase1 (PEPCK1), glucose-6-phosphatase (G6PC), acetyl-CoA carboxylase (ACC), fatty acid synthase (FAS) (P < 0.05) and down-regulated hormone-sensitive lipase (HSL) mRNA expression (P < 0.05) when compared with those of the + B/NR diet group. Taken together, the results indicated that long-term dietary mineral exposure with the commercial supplement level could cause harm to the structure and metabolic function of liver in pigs.