Abstract
Three experiments were conducted to evaluate oil source and peroxidation status (experiment 1) or peroxidized soybean oil (SO; experiments 2 and 3) on growth performance, oxidative stress, and digestibility of dietary ether extract (EE). In experiment 1, palm oil (PO), poultry fat (PF), canola oil (CO), and SO were evaluated, while in experiments 2 and 3, only SO was evaluated. Lipids were either an unheated control (CNT) or thermally processed at 90 °C for 72 hr, being added at 10%, 7.5%, or 3% of the diet in experiments 1, 2, and 3, respectively. In experiment 1, 288 pigs (body weight, BW, 6.1 kg) were fed 1 of 8 factorially arranged treatments with the first factor being lipid source (PO, PF, CO, and SO) and the second factor being peroxidation status (CNT or peroxidized). In experiment 2, 216 pigs (BW 5.8 kg) were fed 1 of 6 treatments consisting of 100%, 90%, 80%, 60%, 20%, and 0% CNT SO blended with 0%, 10%, 20%, 40%, 80%, and 100% peroxidized SO, respectively. In experiment 3, 72 pigs (BW 5.8 kg) were fed either CNT or peroxidized SO. Pigs were fed 21 d with feces collected on day 12 or 14 and pigs bled on day 12 blood collection. In experiment 1, an interaction between oil source and peroxidation status was observed for averaged daily gain (ADG) and average daily feed intake (ADFI; P = 0.10) which was due to no impact of feeding pigs peroxidized PO, PF, or SO on ADG or ADFI compared with feeding pigs CNT PO, PF, or SO, respectively; while pigs fed peroxidized CO resulted in reduced ADG and ADFI compared with pigs fed CNT CO. There was no interaction between oil source and peroxidation status, and no lipid source effect on gain to feed ratio (GF; P ≥ 0.84), but pigs fed the peroxidized lipids had a lower GF compared with pigs fed the CNT lipids (P = 0.09). In experiment 2, feeding pigs diets containing increasing levels of peroxidized SO resulted in reduced ADG (quadratic, P = 0.03), ADFI (linear, P = 0.01), and GF (quadratic, P = 0.01). In experiment 3, feeding peroxidized SO at 3% of the diet reduced ADG (P = 0.11) and ADFI (P = 0.13), with no observed change in GF (P = 0.62). Differences in plasma protein carbonyls, glutathione peroxidase, and vitamin E due to feeding peroxidized lipids were inconsistent across the 3 experiments. Digestibility of dietary EE was reduced in pigs fed peroxidized PO or SO (P = 0.01, experiment 1) and peroxidized SO in experiments 2 and 3 (P ≤ 0.02). In conclusion, the peroxidation status of dietary lipids consistently affects growth performance and EE digestibility but has a variable effect on measures of oxidative stress.