Consumption of highly peroxidized oils has been shown to affect pig performance and oxidative status through the development of compounds which differ according to how oils are thermally processed. The objective of this study was to evaluate the effect of feeding varying degrees of peroxidized soybean oil (SO) on parameters of growth performance; lipid, N, and GE digestibility, gut integrity in growing pigs, and plasma Trp. Fifty-six barrows (25.3 ± 3.3 kg initial BW) were randomly assigned to one of four diets containing either 10% fresh SO (22.5 °C) or thermally processed SO (45 °C for 288 h, 90 °C for 72 h, or 180 °C for 6 h), each with an air infusion of 15 L/min. Peroxide values for the 22.5, 45, 90, and 180 °C processed SO were 2.0, 96, 145, and 4.0 mEq/kg, respectively; 2,4-decadienal values for 22.5, 45, 90, and 180 °C processed SO were 2.11,5.05, 547.62, and 323.57 mg/kg, respectively; and 4-hydroxynonenal concentrations of 0.05, 1.05, 39.46, and 25.71 mg/kg with increasing SO processing temperature. Pigs were individually housed and fed ad libitum for a 49 d period to determine the effects of SO peroxidation status on growth performance, including a metabolism period for assessing GE and N digestibility, and N retention. In vivo urinary lactulose to mannitol ratio was also assessed to evaluate potential changes in small intestinal integrity. Although there were no differences observed in ADFI (P = 0.19), ADG was decreased in pigs fed 90 °C SO diet (P = 0.01), while G:F was increased (P = 0.02) in pigs fed 45 °C SO diet compared to the other SO diets. Pigs fed the 90 °C processed SO had the lowest (P = 0.01) DE as a percentage of GE, whereas ME as a percentage of DE was lowest (P = 0.05) in pigs fed the 180 °C SO and 90 °C SO followed by 45 °C SO and fresh SO. Ether extract (EE) digestibility was lowest (P = 0.01) in pigs fed 90 °C SO followed by pigs fed 180 °C SO, 45 °C SO, and fresh SO. The percent of N retained was greatest (P = 0.01) in pigs fed fresh SO followed by pigs fed 45 °C SO, 180 °C SO, and 90 °C, respectively. There were no differences observed among SO treatments for urinary lactulose to mannitol ratio (P = 0.60). Pigs fed SO processed at 90 °C and 180 °C had lower concentrations (P < 0.01) of serum Trp compared to pigs fed the 22.5 °C and 45 °C SO treatments. The presence of lipid peroxidation products, namely several aldehydes, contained in the 90 °C SO diet reduced ADG, GE and EE digestibility, and N balance, but had no impact on gut permeability.

The objectives of this study were to determine whether feeding thermally processed peroxidized soybean oil (SO) induces markers of oxidative stress and alters antioxidant status in pig tissue, blood, and urine. Fifty-six barrows (25.3 ± 3.3 kg initial BW) were randomly assigned to dietary treatments containing 10% fresh SO (22.5 °C) or thermally processed SO (45 °C for 288 h, 90 °C for 72 h, or 180 °C for 6 h), each with constant air infusion rate of 15 liters/minute. Multiple indices of lipid peroxidation were measured in the SO including peroxide value (2.0, 96, 145, and 4.0 mEq/kg for 22.5, 45, 90, and 180 °C processed SO, respectively) and p-anisidine value (1.2, 8.4, 261, and 174 for 22.5, 45, 90, and 180 °C processed SO, respectively); along with a multitude of aldehydes. Pigs were individually housed and fed ad libitum for 49 d which included a 5 d period in metabolism crates for the collection of urine and serum for measures of oxidative stress. On day 49, pigs were euthanized to determine liver weight and analyze liver-based oxidative stress markers. Oxidative stress markers included serum, urinary, and liver thiobarbituric acid reactive substances (TBARS), and urinary F2-isoprostanes (ISP) as markers of lipid damage; serum and liver protein carbonyls (PC) as a marker of protein damage; and urinary and liver 8-hydroxy-2'-deoxyguanosine (8-OH-2dG) as a marker of DNA damage. Superoxide dismutase (SOD), and catalase activity (CAT) were measured in liver, glutathione peroxidase activity (GPx) was measured in serum and liver, and ferric reducing antioxidant power (FRAP) was measured in serum and urine as determinants of antioxidant status. Pigs fed 90 °C SO had greater urinary ISP (P = 0.02), while pigs fed the 45 °C SO had elevated urinary TBARS (P = 0.02) in comparison to other treatment groups. Pigs fed 45 °C and 90 °C SO had increased serum PC concentrations (P = 0.01) and pigs fed 90 °C SO had greater (P = 0.01) liver concentration of 8-OH-2dG compared to pigs fed the other SO treatments. Furthermore, pigs fed 90 °C SO had reduced serum GPx activity in comparison to pigs fed fresh SO (P = 0.01). In addition, pigs fed 180 °C SO had increased liver CAT activity (P = 0.01). Liver GPx and SOD or serum and urinary FRAP were not affected by dietary treatment. These results indicate that dietary peroxidized soybean oil induced oxidative stress by increasing serum PC while diminishing serum GPx, increasing urinary ISP and TBARS, and increasing 8-OH-2dG and CAT in liver.

An experiment was conducted to evaluate the impact of lipid source on GE and ether extract (EE) digestibility, oxidative stress, and gut integrity in nursery pigs fed diets containing 10% soybean oil (SO), choice white grease (CWG), palm oil (PO), distillers' corn oil with approximately 5% FFA (DCO-1), or distillers' corn oil with approximately 10% FFA (DCO-2). Fifty-four barrows weaned at 28 d of age were fed a common starter diet for 7 d, group fed their respective experimental diets for an additional 7 d, and then moved to metabolism crates and individually fed their respective diets for another 10 d. Following this period, a 4-d total fecal and urine collection period was used to determine apparent total tract digestibility (ATTD) of GE and EE and to determine the DE and ME content of each lipid source (11.03 ± 0.51 kg final BW). Following the last day of fecal and urine collection, pigs were given an oral dose of lactulose and mannitol and fed their respective experimental diets with urine collected for the following 12 h. A subsequent urine collection occurred for 5 h to determine thiobarbituric acid reactive substances (TBARS) and isoprostane (IsoP) concentrations. Following this urine collection, serum was obtained and analyzed for TBARS and endotoxin concentrations. Soybean oil had the greatest ( < 0.05) DE (9,388 kcal/kg) content compared with DCO-1, DCO-2, CWG, and PO (8,001, 8,052, 8,531, and 8,293 kcal/kg lipid, respectively). Energy digestibility was greatest for SO compared with the other lipid sources ( < 0.05). The ATTD of EE averaged 85.0% and varied slightly (84.4 to 85.6%) among treatments. Differences in ME content among lipids were similar to those reported for DE, with ME values for DCO-1, DCO-2, CWG, PO, and SO being 7,921, 7,955, 8,535, 8,350, and 9,408 kcal/kg lipid, respectively. Metabolizable energy as a percentage of DE did not differ among lipid sources. Pigs fed lipid diets had greater ( < 0.05) serum TBARS compared with pigs fed the control diet, but no differences were observed in urinary TBARS excretion among the lipid treatments. Urinary IsoP excretion differed among treatments ( < 0.01) but was highly variable (34.0 to 104.6 pg). However, no differences were observed among treatments for the urinary lactulose:mannitol ratio and serum endotoxin. These results indicate that DE and ME content of SO are greater than that of other lipid sources evaluated, but feeding these lipids has no effect on gut integrity while producing variable effects on oxidative stress.

The objectives of the current experiments were to evaluate the effect of feeding soybean oil (SO) with different levels of peroxidation on lipid, N, and GE digestibility, gut integrity, oxidative stress, and growth performance in nursery pigs. Treatments consisted diets containing 10% fresh SO (22.5 °C) or thermally processed SO (45 °C for 288 h, 90 °C for 72 h, or 180 °C for 6 h), each with an air infusion of 15 L/min, with postprocessing peroxide values of 7.6, 11.5, 19.1, and 13.4 mEq/kg and p-anisidine values of 1.92, 6.29, 149, and 159, for the 22.5 °C, 45 °C, 90 °C and 180 °C processed SO, respectively. In experiment 1, 64 barrows (7.1 ± 0.9 kg initial BW) were randomly allotted into 2 rooms of 32 pens and individually fed their experimental diets for 21 d, with a fresh fecal sample collected on day 20 for determination of GE and lipid digestibility. In experiment 2, 56 barrows (BW 9.16 ± 1.56 kg) were placed into individual metabolism crates for assessment of GE, lipid, and N digestibility and N retention. Urinary lactulose to mannitol ratio was assessed to evaluate in vivo small intestinal integrity, and urine and plasma were collected to analyze for markers of oxidative stress. Pigs were subsequently euthanized to obtain liver weights and analyze the liver for markers of oxidative stress. In experiment 1, pigs fed the SO thermally processed at 90 °C had reduced ADG (P = 0.01) and ADFI (P = 0.04) compared to pigs fed the other SO treatment groups, with no differences noted among pigs fed the 22.5 °C, 45 °C, and 180 °C SO treatments. No effects of feeding thermally processing SO on dietary GE or lipid digestibility (P &gt; 0.10) were noted in either experiment. In experiment 2, there was no dietary effect of feeding peroxidized SO on the DE:ME ratio, N digestibility, or N retained as a percent of N digested, on the urinary ratio of lactulose to mannitol, on serum, urinary, or liver thiobarbituric acid reactive substances, on plasma protein carbonyls, or on urinary or liver 8-OH-2dG (P &gt; 0.10). In experiment 2, pigs fed the SO thermally processed at 90 °C had the greatest isoprostane concentrations in the serum (P ≤ 0.01) and urine (P ≤ 0.05) compared to pigs fed the unprocessed SO. These results indicate that the change in fatty acid composition and/or the presence of lipid peroxidation products in peroxidized SO may reduce ADG and ADFI in nursery pigs, but appears to have no impact on GE, lipid, or N digestibility, or gut permeability. These data suggest that the presence of lipid peroxidation products may affect certain markers of oxidative stress.

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important lipid peroxidation products that need to be measured as suggested by their consistent correlations with growth performance and oxidative status in swine and poultry. Additionally, these experiments and a review of literature indicate that markers of oxidative stress that should be measured include ISP and 8-OH-2dG in urine (pigs), and PC and GPx in blood (pigs and poultry). Overall, this thesis showed that oil quality should not be underestimated in livestock production. Feeding peroxidized oils can induce oxidative stress and antagonizes growth performance and digestibility in swine and poultry. CHAPTER 1 LITERATURE REVIEW were no differences observed among SO treatments for urinary lactulose:mannitol ratio (P = 0.60). These results indicate that the presence of compounds such as PV, DDE, and HNE contained in the 90 o C SO diet reduce ADG as well as reduce GE and ether extract digestibility, and N balance, but appear to have no impact on gut permeability.

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.