Abstract: Reactive oxygen metabolites (ROMs) are continuously produced as by-products of mitochondrial respiration and periodically change during inflammatory reactions (Aw, 1999). The gastrointestinal system is not only a metabolically active site, but also a site of action between the host and the microorganism, so it usually leads to an inflammatory reaction. Oxidation of dietary components can imbalance the body's oxidation and antioxidant system, consuming endogenous antioxidants, leading to apoptosis and local tissue necrosis. The addition of exogenous antioxidants can reduce the consumption of endogenous antioxidants and alleviate the effects of oxidative stress on the development and function of the gastrointestinal system. 1. The production of reactive oxygen species and the formation of oxidative damage In the process of normal metabolism and innate immune response, cells also produce reactive oxygen metabolites (ROM) - free radicals. First, the active metabolism of intestinal epithelial cells is itself a source of ROM, and its production is related to the activity of the electron transport chain (Ojano-Dirain et al., 2007). The active substances produced include superoxide anions (O2,), hydrogen peroxide (H2O2) and hydroxyl radicals (·OH), which are inevitable products of oxidative phosphorylation in mitochondria (Chance et al., 1979). Second, another endogenous oxidative stress stems from the innate congenital and acquired immune system producing nitric oxide (NO) during the reaction with many commensal and pathogenic microorganisms, which is in the process of food and water absorption. Inevitably will happen. However, it is currently uncertain whether nitric oxide damages inflammatory tissue or affects the expression of inflammatory cells, and it interacts with superoxide anions to produce peroxynitrite anion (ONOO-) with longer half-life and higher fat solubility. Diffusivity causes greater damage to reactive nitrogen metabolites (Kruidinier and Verspaget, 2002). These metabolites destroy the structure and function of various macromolecular substances, including lipid membranes, proteins (such as enzymes), and DNA. In addition, in vitro studies have shown that low doses of ROM or endogenous antioxidant (AOX) depletion can lead to apoptosis. Apoptosis differs from tissue necrosis, and their differences in morphological and biochemical properties ultimately lead to cell rupture and autologous digestion. Kruidinier and Verspaget (2002) showed in vitro studies that the addition of AOX compounds can prevent apoptosis. The ROM protects cells from damage through an endogenous antioxidant defense system. This defense system consists of three classes of antioxidants (Miller et al., 1993): the first group is an enzyme antioxidant, including mitochondrial Mn-dependent superoxide dismutase (SOD) expression, Cu-Zn-dependent SOD and Se-dependent Glutathione peroxidase (GSH-Px, Aw, 1999). Enzyme antioxidants are the primary endogenous antioxidant defense system and the first line of defense against ROMs such as H2O2 and ·OH. The second group is a protein antioxidant of the intracellular fluid, such as albumin, cysteine ​​and homocysteine ​​with a thiol group. The third group is low molecular weight short chain antioxidants such as water soluble vitamin C, glutathione, fat soluble vitamin E and A. If oxidative stress exceeds the animal's antioxidant capacity, tissue damage will be further amplified (Weiss, 1989). 2. The cause of oxidative stress Oxidative stress is produced in many cases of agricultural production. During disease infection, the animal's first immune response causes ROM and neutrophils to produce ROM, thereby killing pathogenic microorganisms, while antioxidant enzymes such as SOD and GSH-Px clear ROM to prevent damage to the host. cell. The inflammatory response of the intestinal system usually reduces the antioxidant capacity of the animal, leading to malabsorption of certain nutrients, particularly in the absorption of fat-soluble vitamins (Miller et al., 1993). Environmental conditions also cause oxidative stress in animals. Bernabucci et al. (2005) studied the effects of oxidative stress on perinatal dairy cows in spring or summer (39.5 C; temperature and humidity index of 73), indicating oxidized lipids (TBARS) in red blood cells of perinatal dairy cows during summer. SOD levels are higher than spring. Lin et al. (2006) also found that acute heat stress in broiler production can induce oxidative stress, which is characterized by elevated levels of TBARS in plasma and decreased AOX enzyme activity in plasma and liver. Mujahid et al. (2007) reported that ROM content in muscle mitochondria of meat males increased under heat stress conditions, which is different from egg chicks under the same conditions. Bottje et al. (1998) compared oxidative and reduced glutathione ratios (GSSG/GSH) in broilers under poorly ventilated and well ventilated environmental conditions, indicating that a greater degree of oxidative stress leads to oxidized glutathione. The level rises. 3. The source of free radicals in the diet The fat added to the diet is an important source of free radicals or ROM. Novus International surveyed the different types of fats collected in 2000-2005 and found that 40-50% of the fat used in animal diets is unstable, which is higher in the hot summer months. In addition to the fat added directly to the diet, approximately 50% of the dietary lipids are derived from other feed ingredients such as cottonseed meal, vinasse, cardamom and fish meal. Most of the lipids from these feed ingredients contain large amounts of unsaturated fatty acids that are easily oxidized. For example, the distiller's grains produced in the ethanol production process are the main source of unsaturated fatty acids. The heat in the distillation process and the high moisture in the wet distiller's grains exacerbate the oxidation process of unsaturated fatty acids, eventually leading to more kernum. Easy to oxidize and unstable fat. By reacting with free radicals, antioxidants in the diet can reduce the peroxide carrier and convert it into non-toxic metabolites. In terms of lipid membranes, antioxidants can bind to fatty acids that are susceptible to oxidation, thereby stabilizing the molecular structure, inhibiting the oxidation of lipids and further formation of peroxides. Dietary antioxidants containing hydrogen-containing active groups such as ethoxyquin, tert-butyl hydroquinone (tBHQ), butylated hydroxytoluene (BHT) or butylated hydroxyanisole (BHA), can be asymmetric with fatty acids or media The electron radicals combine to prevent them from being oxidized. The addition of AOX stabilizes the fat in the wet mash and prevents further oxidation and loss of the unsaturated fatty acids C18:2 and C18:3 (Andrews and Vázquez-A?ón). At the same time, AOX can effectively inhibit the energy loss caused by the oxidation process of fat. The energy values ​​determined by atomic calorimetry indicate that the energy of oxidized fat is reduced by 35% compared to fresh fat. However, in the presence of an effective AOX, the energy value is maintained. Oxidation of fat not only reduces its energy and biological value, but also extends the oxidation reaction to other lipid components such as vitamins and dietary pigments. 4. Animal response to antioxidants in the diet Oxidation of dietary ingredients is not simply a reduction in the nutritional value of the diet, but a more severe lipid peroxidation in liver tissue can disrupt the redox balance in epithelial cells. Wang et al (2000) found in vitro that it can cause apoptosis of CaCo-2 cells and reduce the GSH/GSSG value at the beginning of the reaction. This result is consistent with the results observed in human T cells, which can cause apoptosis in activated T cells (Chang et al., 2002). The importance of exogenously adding AOX to improve the stability of the diet is that it can protect AOX in the intestinal lumen. Synthesizing AOXs can reduce the absorption of endogenous AOXs such as glutathione, vitamins A and E by intestinal cells. This view has been confirmed in broiler studies by adding ethoxyquin to normal diets or diets containing oxidized fat, resulting in increased levels of glutathione in duodenal tissues of broilers (Wang et al., 1997). . Not to mention fat oxidation, even if fresh fat is added to the diet, the ROM level in the intestine is sufficient to consume a sufficient amount of AOX. Glutathione and other endogenous AOXs will inhibit ROS production through ethoxyquinoline metabolism. In intestinal epithelial cells, the important role of maintaining redox stability is related to ROM as a regulator of signaling pathways for apoptosis (Haddad, 2004). Therefore, they can shorten the half-life of host cells, resulting in reduced feed efficiency and inflammation or infection (Ojano-Dirain et al., 2007). The purpose of this pilot study was to investigate the effects of oxidized fat on the gastrointestinal system and to determine whether the addition of AOX to the diet can improve ROS-related cellular changes. Data from the early stages of hatching indicate that AOXs are not only beneficial to the function of the intestines and the development of the immune system, but also beneficial to the growth and development of the chickens. Dibner et al. (1996) studied the effects of oxidized fat on the related functions of the intestinal system through various metabolic, microbiological and histological techniques. Histopathological changes were used to measure intestinal structure, while nutrient uptake was used to measure gastrointestinal function. Furthermore, in gastrointestinal epithelial cells and intestines, proliferation of stem cells is associated with lymphoid tissue and is used to assess cytotoxicity and immune status. In this trial, the broiler chickens were fed a standard corn-soybean pre-fed diet with fat in the form of a mixture of oxidized fat and non-oxidized fat to meet the peroxide requirements in the diet. The initial peroxide value (IPV) of non-oxidized poultry fat was 1.04 meq/kg, the oxidized poultry fat was 212.5 meq/kg, and the lard was 3.2 meq/kg. The treatment group consisted of a non-oxidized fat addition group; the non-oxidized fat group was supplemented with 125 ppm (125 g/ton) ethoxyquinoline (antioxidant for mountain quinquina ethoxyquinoline feed); oxidized fat addition group and oxidation Ethoxyquinoline was added to the fat group. The fat source of this test was poultry fat and lard, which was added to two oxidized fat treatment groups to achieve a peroxide level of 4.2 meq/kg in the final feed. The test was divided into 3 cages, 8 chickens per cage, and 4 diets were randomly fed and fed ad libitum. Body weight and consumption of broilers at 7, 14 and 21 days old were measured. Test animals were randomly selected from each group to determine intestinal microbes, nutrient uptake rates, and pathological changes. Part of the trial data for the two- to three-week period of this trial has been published, which contains a more detailed description of the test method (Dibner et al., 1996; Sherme et al., 1995). Figure 1 Effect of adding fresh fat, fresh fat + ethoxyquinoline, oxidized fat, oxidized fat + ethoxyquinoline on the ileal histomorphology of 11-day-old broiler broiler The fat oxidation shown in Figure 1 and the protective effect of AOX on the ileum of young animals showed that there were significant differences in intestinal development between 11-day-old broilers treated with different diets. The addition of oxidized fat to the diet slowed the growth of intestinal villi (single factor comparison, P < 0.05), but had no effect on crypt depth (P = 0.27). It was shown that the addition of fresh fat could increase the proliferative activity of crypt hepatocytes compared with the addition of oxidized fat, while AOX in the diet significantly reduced the extent of this effect (P < 0.05). The results of this trial are consistent with previously reported results that reduce the lifespan of adult chicken epithelial cells (Dibner et al., 1996). In addition, the oxidized fat addition group was compared with the fresh fat addition group (P < 0.17), the ethoxyquinoline addition group was compared with the control group (P = 0.05), and the cecal tonsil diameter decreased at 11 days of age, indicating The development of immune organs is also inhibited. Histological examination showed that the proliferation of bursal lymphocytes may be related to tonsil developmental delay (data not shown). Studies have shown that oxidative feed ingredients can shorten cell life, which is consistent with the role of ROM in cell apoptosis reported by Haddad (2004). AOXs have a beneficial effect on fresh fat, indicating that the metabolic ROS produced during mitochondrial respiration can meet the system's own needs under a large number of oxidative stress conditions. The addition of ethoxyquinoline to fresh fat or oxidized fat diets significantly increased vitamin A content in the liver (Table 1), which supports the hypothesis that synthetic AOXs can save on endogenous AOXs consumption. Therefore, even if AOX is added to a diet containing fresh fat, the consumption of endogenous AOX can be saved. 5. Conclusion The need to ensure high fat diet ingredients has long been recognized. Under these circumstances, the main role of adding AOX is to protect the nutrients and energy in the feed, so that the value of the feed ingredients can be maximized and maximize economic benefits. The potential role of ROM in diets for gastrointestinal structure and function is generally overlooked, and this test fully demonstrates that AOXs in feeds relieve some of the oxidative stress in the gastrointestinal tract and save on oxidative stress. The supply of sex AOX. References Aw, T. (1999). Molecular and cellular responses to oxidative stress and changes in oxidation-reduction imbalance in the intestine. Am. J. Clin. Nut. 70: 557-565. Bernabucci, U., B. Ronchi, and A. Nardone. (2005). Influence of body condition score on relationships between metabolic status and oxidative stress in periparturient dairy cows. J. Dairy. Sci. 88:2017-2026. Bottje, WG, S. Wang, FJ Kelly, C. Dunster, A. Williams, and I. Mudway. (1998). Antioxidant defenses in lung lining fluid of broilers: impact of poor ventilation conditions. Poultry Sci. 77:516- 522. Cabel, MC and PW Waldroup, WD Shermer, and DF Calabotta. 1988. Effects of Ethoxyquin feed preservative and peroxide level on broiler performance. Poultry Sci. 67. Chance, B., Sies, H. and Boveris, A. (1979). Hydroxide metabolism in mammalian organs. Physiol. Rev. 59: 527-609. Chang, W.-K., Yang, K., Chuang, H., Jan, J.-T. and Shaio, M.-F. (2002). Glutamine protects activated human T cells from apoptosis by up-regulating glutathione And Bcl-2 levels. Clin. Immun. 104: 151-160. Dibner, J., Atwell, C., Kitchell, M., Shermer, W. and Ivey, F. (1996). Feeding of oxidized fats to broilers and swine: effects on enterocyte tunover, hepatocyte proliferation and the gut associated lymphoid tissue Anim. Feed Sci. Technol. 62: 1-13. Haddad, J. (2004). Redox and oxidant-mediated regulation of apoptosis signaling pathways: immuno-pharmaco-redox conception of oxidative siege versus cell death commitment. International Immunopharmacology 4: 475-493. Kruidinier, L. and Verspaget, HW (2002). Review article: Oxidative stress as a pathogenic factor in inflammatory bowel disease – radicals or ridiculous?. Aliment Pharmacol. Ther. 16:1997-2015. Lin, H., E. Decuypere, and Johan Buyse. (2006). Acute heat stress induces oxidative stress in broiler. Comp. Biochem. and Physiol. Part A 144: 11-17. Miller JK and E. Brezeinska-Slebodizinska. (1993). Oxidative Stress, Antioxidants and Animal Function. J. Dairy Sci. 76:2812-2823. Mujahid, A., Y. Akiba, and M. Toyomizu. (2007). Acute heat stress induces oxidative stress and reducing adaptation in young white leghorn cockerels by down regulation of avian uncoupling protein. Poultry Sci 86:364-371. Ojano-Dirain, C., Tinsley, N., Wing, T., Cooper, M. and Bottje, W. (2007). Membrane potential and H2O2 production in duodenal mitochondria from broiler chickens with low and high feed efficiency. Comp. Biochem. Physiol. Part A, 147: 934-941. Shermer, W., Ivey, F., Andrews, J., Atwell, C., Kitchell, M. and Dibner, J. (1995). Feeding of oxidized fats to broilers: Poor performance is associated with functional changes in the gastrointestinal System. J Australia Poultry Sci, 7: 153-159. Sordillo, LM, K. Shafer-Weaver, and D. DeRosa. (1997). Immunobiology of the mammary gland. J. Dairy Sci. 80:1851-1865. Wang, S.-Y., Bottje, W., Maynard, P., Dibner, J. and Shermer, W. (1997). Effect of Santoquin and oxidized fat on liver and intestinal glutathione in broilers. Poultry Sci. 76: 961-967. Wang, T.-G., Gotoh, Y., Jennings, M., Rhoads, C. and Aw, T. (2000). Lipid hydroperoxide-induced apoptosis in human colonic CaCo-2 cells is associated with an early loss of Financial redox balance. FASEB J. 14: 1567-1576. Weiss, S. (1989). Tissue destruction by neutrophils. N. Engl. J. Med. 3220: 365-376
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