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Rao, Prakash, Raju, Panda, Poonam, and Murthy: Effect of Supplementing Organic Selenium on Performance, Carcass Traits, Oxidative Parameters and Immune Responses in Commercial Broiler Chickens


An experiment was conducted to determine the effect of supplementing various concentrations (0, 100, 200, 300, or 400 μg/kg diet) of organic Se on growth performance, carcass traits, oxidative stress, and immune responses in commercial broiler chickens reared in open-sided poultry house under tropical climatic conditions. Each diet was fed ad libitum to eight replicates consisting of six birds in each pen from 1 to 42 d of age. Body weight gain and feed efficiency, and relative weight of liver, abdominal fat and ready to cook yields were not affected (p>0.05) by organic Se supplementation to broiler diets. Lipid peroxidation in plasma decreased, while activities of glutathione peroxidase and glutathione reductase in plasma increased (p<0.01) linearly with Se concentration in diet. The ratios between heterophyls and lymphocytes and relative weight of lymphoid organs (bursa, spleen, and thymus), and antibody production to Newcastle disease vaccination were not affected (p>0.05) by Se supplementation to broiler diets. However, the cell-mediated immunity (lymphocyte proliferation ratio) increased (p<0.01) linearly with dietary Se concentration. The results of the present study indicate that the supplementation of Se did not influence body weight and feed efficiency. However, supplementation of Se increased antioxidant status and lymphocyte proliferation in broiler chickens.


Genetic selection for higher growth rate, and providing balanced diet and superior health care measures led to a higher body weight in commercial broilers. The birds that are being reared in open-sided poultry houses may lead to stress due to constant dynamic variations in temperature and humidity in the environment, which causes adverse effects on performance (Niu et al., 2009), meat quality and immune responses (Thompson and Scott, 1970). Further, heat causes a major stressor for chicken due to their high metabolic rate, and body temperature and lack of sweat glands (Sahin and Kucuk, 2003). High environmental temperature in the tropical countries causes heavy financial losses to poultry due to reduced feed intake and decreasing feed conversion efficiency (Panda et al., 2008). However, theses adversities in the tropics can be minimized by feeding diet supplemented with organic selenium (Se).
Se is a trace mineral that is essential to keep good health for animals and humans. Deficiency of Se results in exudative diathesis and pancreatic degeneration (Toghyani et al., 2008), and it plays an important role in immune function and production of immunoglobulin (Spallholz et al., 1973). Supplementation of Se in chicken diet increases antibody titers to Newcastle disease (ND) (Hegazy and Adachi, 2000). Further, Se influences immune responses through its incorporation into selenoproteins such as the amino acid selenocysteine (Hoffmann, 2007).
The biological systems are continuously influenced to free radicals and reactive oxygen species (ROS), which are produced as a part of the normal cell metabolism (Tappel and Tappel, 2004). Furthermore, in a several physiological and pathological states, excess amounts of ROS are generated (Fridivich, 1978), which damages the cell phospholipid membranes and other macromolecules (Wiseman and Halliwell, 1996). Utilization of appropriate antioxidants will help the biological system by scavenging reactive oxygen, which intern reduces lipid peroxidation (LP) and increase activity of antioxidant defense system (Nunes et al., 2005).
The ideal Se concentration in the diet is essential for the normal development and functioning of the immune system (Koski and Marilyn, 2003) and for maintaining the systemic defense in broilers reared in tropics. However, information about the beneficial effects of supplementation of Se in maize and soybean meal-based diets on performance of broiler reared in tropics is scanty. Therefore, an experiment was conducted to study the effects of supplementing Se on performance, slaughter parameters, stress indices, and immune responses in commercial broilers.


Experimental birds, management, and diets

Day-old commercial female broiler chicks (n = 240) were distributed randomly into eight replicates of five treatments with six chicks in each replicate (pen). On day one, chicks were wing banded and housed in wire-floored stainless steel battery brooders. The brooder temperature was maintained at 35±0.5°C until 7 d of age and gradually decreased to 27°C by 21 d of age, after which, chicks were maintained at room temperature (20 to 27°C). Birds were vaccinated against Newcastle (7th and 28th d) and infectious bursal diseases (15th d) as per the standard vaccination schedule. The experimental protocol was approved by the institute animal ethics committee.
Maize and soybean meal-based diets were prepared to contain 2,944, 3,049 and 3,150 kcal ME/kg during the pre-starter (1 to 11 d), starter (12 to 21 d), and finisher (>22 d of age) phases, with respective crude protein contents of 23, 21, and 19 g/100 g feed (Table 1). The maize and soybean meal were analyzed for amino acid concentrations (Llames and Fontaine, 1994). The analyzed amino acid composition was utilized for formulating the experimental diets. Further, the diets were supplemented with organic Se (MinPlex Selenium, Bentoli AgriNutrition, Homestead, Florida, USA) to arrive five graded concentrations in diet I (basal diet without organic Se); diet II (diet I+organic Se at 100 μg/kg diet); diet III (diet I+organic Se at 200 μg/kg diet); diet IV (diet I+organic Se at 300 μg/kg diet); diet V (diet I+organic Se at 400 μg/kg diet), and each diet was allotted at random to eight replicates and fed ad libitum from 1 to 42 d of age. The weighed amount of organic Se was incorporated in the premix for various diets in order to attain the desired concentration and finally the premix was thoroughly mixed with the respective diets using stainless steel double cone blenders with 300 rpm for 3 min.

Productive performance and carcass parameters

Body weight and feed intake were recorded at 21 and 42 d of age, and feed efficiency per pen was calculated as body weight gain per unit feed intake.
At 42 d of age, eight birds from each treatment weighing near to the mean body weight (±5%) of the respective group were selected and removed from feed for 12 h to record body weight loss during pre-slaughter holding period. The birds were slaughtered by cervical dislocation to study carcass traits. Ready to cook yield (including giblet) and relative weight of breast, abdominal fat, and liver were recorded and expressed as grams per kilogram pre-slaughter live body mass of the respective bird.

Stress parameters

Stress responses in terms of LP, activities of certain antioxidant enzymes, and HL ratio in peripheral blood smears were studied. Approximately 4 ml of blood was drawn from the brachial vein of eight birds per treatment on 35th d of age into a centrifuge tube containing citrate buffer (citrate 0.8 g/100 ml and 1.5 ml/10 ml blood) for erythrocyte separation and enzyme estimation. Blood samples were centrifuged at 500×g for 15 min at 4°C to separate the buffy coat and RBC pellet. The RBC were washed thrice with PBS (pH 7.4). The RBC pellet was mixed with an equal volume of PBS, and then lysed using distilled water (RBC to distilled water, 1:20) and the same procedure was applied for quantifying the LP (Ohkawa et al., 1979), activity of RBCC (Berg Meyer, 1983). The degree of peroxidation was expressed as nanomoles malonyl dialdehyde (MDA)/milligram protein and the RBCC activity as units per gram of hemoglobulin, respectively. The hemolysate was also analyzed for the activities of GSH Rx (Cohen et al., 1970) and GSH Px (Paglia and Valantine, 1967), which were expressed as units/milliliter. At 42 d of age, blood smears (eight birds from each treatment) were prepared and stained with Giemsa, and 100 cells were counted to calculate HL ratio.

Immune responses

The effect of supplementing Se on humoral (ND virus) and cell-mediated (LPR) immune responses were studied. Blood samples were collected from one bird from each pen (eight birds from each treatment) on the 40th d of age to study the LPR and antibody titres against NDV.

In vitro LPR

In vitro LPR was determined using the mitogen Concanavalin A (Con A) and determined as LPR between the proliferation of mitogen-stimulated and unstimulated cells. The LPR was measured using 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) salt (Bounous et al., 1992). At 40 d of age, approximately 2 ml blood was collected from the brachial vein of the bird from each replicate and transferred to a centrifuge tube containing 5 mg heparin disodium salt. The unclotted blood sample was layered gently over histopaque 1077 (Sigma, Mumbai, India) and centrifuged at 500×g for 20 min at 4°C. The cellular band at the interface was collected and transferred to another tube and washed three times with RPMI 1640 medium (AL 028A, Himedia, India). Numbers of viable cells were determined by using the trypan blue dye exclusion method, and cell concentration was adjusted to 1×107 cells/ml of RPMI 1640 medium. A sample of cells (105 purified lymphocytes) was used to measure lymphocyte proliferation by adding 10 μl of suspension to each well of a 96-well flat bottom sterile tissue culture plate. Con A (0.9 μg in 150 μl RPMI/well) was added to those cells to be stimulated. A similar volume of RPMI was added to the unstimulated cultures. The plate was incubated at 37°C and 5% CO2 concentration for 69 h in a humid atmosphere, then 20 μl MTT (10 mg/ml) was added to each well, and the plate was incubated for 3 h. At 72 h, 100 μl of 1 M HCl-isopropanol (4%) was added to each well and mixed thoroughly with a micropipette to dissolve the formazan crystals, which gave a deep purple color. The color intensity was measured in an enzyme-linked immunosorbent assay (ELISA) reader (V. 200.1, μ Quant; Biotek Instruments, Inc., USA) at 550 nm. The LPR was calculated as (OD of Con A well-OD of without Con A well)/OD of unstimulated cells.

Antibody titre to ND vaccine

Broilers were vaccinated against ND by ocular route at the 7th and 28th d of age with Lsota strain (ND Lasota Vac-500; Indivax Pvt., Ltd., Hyderabad, India). At 40 d of age, blood was collected and a serum was separated. Antibody titres against ND vaccine were measured with ELISA (96-6547; Synbiotics, San Diego, CA, USA).

Statistical analysis

The data were subjected to regression analysis considering the levels of Se as independent variable and various parameters (production, slaughter, stress, and immune responses) as dependent variables to know the relation (linear or nonlinear) between independent and dependant variables using SPSS software (SPSS Version 12; South Asia Pvt., Ltd., Bangaluru, India).


Productive performance and carcass traits

The results of the present study showed the body weight gain, feed efficiency and slaughter traits (relative weight of ready to cook, giblet, liver, abdominal fat, spleen, bursa, breast muscle and thymus) were not affected (p>0.05) with Se supplementation (Table 2). The similar results have been reported, wherein Se supplementation revealed insignificant effects on body weight gain and feed efficiency (Downs et al., 2000; Choct et al., 2004; Payne and Southern, 2005; Perić et al., 2009) in broilers. On the contrary, it has been reported that the improved body weight and feed efficiency in chicken reared under the heat stress, when fed diet supplemented with Se (Christine et al., 2002; Niu et al., 2009; Ibrahim et al., 2011). Similarly, increased feed efficiency and body weight gain is reported in broilers chicken fed diet supplemented Se-enriched yeast (Krstic et al., 2012). The insignificant difference in body weight gain, feed efficiency and other slaughter parameters in the present study might be due to feeding the balanced diet with adequate nutritional practice (Lesson and Summer, 2001).

Stress parameters

LP decreased linearly (p<0.01) with each increment of Se in diet (Table 3). On the contrary, the activities of glutathione peroxidase (GSH Px), glutathione reductase (GSH Rx) and red blood cell (RBC) catalase (RBCC) increased linearly (p<0.01) with increase in Se concentration in diet. However, variation in concentration of Se in diet did not influence (p>0.05) the heterophyl to lymphocyte (HL) ratio in broilers. It is well established that the LP, a process involved in degradation of structural components of cell membranes (Kuhn and Borchert, 2002; Georgieva et al., 2011) and ROS accumulation is known to induce LP and oxidative stress (Devi et al., 2000). Whereas, the RBCC, GSH Px and GSH Rx protects the biological cells from the adversities of ROS (Georgieva et al., 2011). GSH Px and GSH Rx are well known for catalyzing the reduction of hydrogen peroxide and organic hydroperoxides, thus protecting cells from oxidative damage (Papp et al., 2007). In the present study, decreased LP and increased activities of the above antioxidant enzymes suggest that Se supplementation progressively reduced oxidative stress with gradient increase in dietary Se concentration (Cave et al., 2006) in broiler. The cell-mediated immune response (LPR) increased significantly with the concentration of Se in broiler diet. Similar findings are also reported in domestic animals (Finch and Turner, 1996), humans (McKenzie et al., 1998) and broilers (Singh et al., 2006) fed diets with Se supplementation.

Immune responses

Selenium is an important for optimum immune response, and it influences the innate and acquired immune systems. Effect of dietary Se concentration on antibody titres to ND vaccine and lymphocyte proliferation ratio (LPR) in commercial broilers is presented in Table 4. Antibody titres against ND vaccine was not affected (p>0.05) by feeding the diet containing varying concentration of Se, which might be due to ideal ambient temperature during finisher phase. Contrary, in vitro cell-mediated immune response (LPR) increased linearly (p<0.001) with increasing the concentration of Se (up to 400 μg/kg) in broiler diet. The immune modulator effect of Se might have mediated through reduction of stress in chicken as evident by increased antioxidant (GSH Px, GSH Rx, and RBCC) and decreased LP in the present study. Similarly, it has also been reported that Se or vitamin E greatly influences the humoral immune response up to 30 wks of age (Marsh et al., 1981), but not during the later phase in broilers. Similarly, Zhang et al. (2012) reported that the selenium supplementation in the chicken diets improved the immunological parameters. Further, they reported that the deficiency in Se in the diets results in increased levels of oxidative stress and its related diseases. However, the lack of response in humoral immunity in the present study might be due to the study of the parameter was carried out at the latter phase of the broiler growth.


Based on the results, it is concluded that supplementation of Se did not influence body weight and feed efficiency. However, Se supplementation (up to 400 μg/kg diet) increased anti-oxidant status (reduced LP and increased activities of GSH Px, GSH Rx, and RBCC) and LPR.

Table 1
Ingredient and nutrient content of the basal diets
Pre-starter Starter Finisher

Age (d)

1–11 12–21 22–42
Ingredients (%)
  Maize 50.1 54.7 60.1
  Soybean meal, 46% CP 42.2 36.7 31.1
  Sunflower oil 3.58 4.36 4.85
  Common salt 0.35 0.35 0.35
  Sodium bicarbonate 0.1 0.1 0.1
  Dicalcium phosphate 1.93 1.97 1.71
  Oyster shell grit 0.97 1.01 0.93
  DL-methionine 0.17 0.15 0.13
  L-lysine HCl 0 0.042 0.077
  Premixa 0.55 0.55 0.55
Nutrient content (dry matter basis)
  Metabolizable energyb (kcal/g) 2.94 3.05 3.15
  Crude proteinc (%) 23.0 21.0 19.0
  Lysined (%) 1.30 1.19 1.07
  Methionined (%) 0.51 0.46 0.42
  Calciumb (%) 0.89 0.88 0.78
  Non-phytate phosphorusb (%) 0.45 0.45 0.40

Diet I (basal diet without organic Se); Diet II (Diet I+organic Se at 100 μg/kg diet); Diet III (Diet I+organic Se at 200 μg/kg diet); Diet IV (Diet I+organic Se at 300 μg/kg diet); Diet V (Diet I+ organic Se at 400 μg/kg diet)

a Premix provided (in milligrams/kilogram diet): thiamin 1; pyridoxine, 2; cyanocobalamine, 0.01; niacin, 15; pantothenic acid, 10; α-tocopherol, 10 IU; riboflavin, 10; biotin, 0.08; menadione, 2; retinol acetate, 2.75; cholecalciferol, 0.03; choline, 650; copper, 8; iron, 45; manganese, 80; zinc, 60; selenium, 0.18; monensin sodium, 50; hydrated sodium calcium alumino silicates, 800.

b Calculated values.

c Analyzed values.

d Calculated based on analyzed ingredient composition.

Table 2
Effect of dietary Se concentration (μg/kg) on various slaughter traits (g/kg pre-slaughter live body eight) and performance in broiler chicks (1 to 42 d of age)
Se (μg/kg diet) Body weight (g) FCR Holding losses RTC Giblet Liver Abdomin al fat Spleen Bursa Brest muscle Thymus
0 2,295 1.756 79.4 690.5 43.17 22.43 16.18 1.369 1.242 163.2 2.129
100 2,323 1.766 62.4 688.3 42.58 20.79 16.97 1.260 1.692 158.6 2.576
200 2,336 1.736 49.6 685.6 42.31 21.02 16.93 1.317 1.537 161.2 2.768
300 2,296 1.743 43.1 683.1 41.81 20.75 18.24 1.674 1.356 160.6 2.509
400 2,257 1.781 28.9 686.3 41.48 19.45 14.20 1.080 1.474 160.9 2.442
SEM 15.28 0.012 2.75 2.84 0.54 0.47 0.92 0.09 0.08 1.76 0.10
p value
  Linear 0.345 0.770 0.01 0.50 0.28 0.06 0.68 0.801 0.82 0.85 0.46
  Quadratic 0.228 0.709 0.01 0.72 0.56 0.16 0.52 0.66 0.59 0.89 0.18

Each mean represents the data from eight chicks.

RTC = Ready to cook yield. SEM = Standard error mean. FCR = Feed conversion ratio.

Table 3
Stress parameters in broilers (6 wks of age) fed with different concentrations of Se in the diet
Se (μg/kg diet) HL ratio LP (nmol MDA/mg protein) RBCC (units/g Hb) GSH Px (units/ml) GSH Rx (units/ml)
0 0.403 1.756 303.3 206.3 65.33
100 0.355 1.630 353.1 230.7 71.26
200 0.455 1.588 333.6 245.8 83.76
300 0.419 1.435 370.1 260.3 82.20
400 0.379 1.370 422.4 277.3 85.85
SEM 0.01 0.02 7.60 4.21 1.55
p value
  Linear 0.806 0.001 0.001 0.001 0.001
  Quadratic 0.285 0.001 0.001 0.001 0.001

Each mean represents the data from eight chicks.

GSH = Px glutathione peroxidase. GSH = Rx glutathione reductase. H:L = Heterophyl to lymphocyte. LP = Lipid peroxidation. RBCC = RBC catalase. SEM = Standard error mean.

Table 4
Antibody titres to Newcastle disease vaccine and lymphocyte proliferation ratio in commercial broilers fed with different concentrations of Se in diet
Se (μg/kg diet) ND titre, ELISA LPR
0 8,028 0.400
100 6,484 0.489
200 7,244 0.546
300 7,389 0.564
400 8,756 0.614
SEM 646 0.02
p value
  Linear 0.61 0.001
  Quadratic 0.57 0.001

Each mean represents the data from eight chicks

ELISA = Enzyme linked immunesorbent assay. LPR = Lymphocyte proliferation ratio. ND = Newcastle disease. SEM = Standard error mean.


Berg Meyer HU. 1983. Catalase. Methods of enzymatic analysis. Berg Meyer HU, editor2:Verlag Chemie; Weinheim: p. 165–166.

Bounous DI, Campagnoli RP, Brown J. 1992. Comparison of MTT colorimetric assay and tritiated thymidine uptake for lymphocyte proliferation assays using chicken splenocytes. Avian Dis 36:1022–1027.
crossref pmid
Cave AC, Brewer AC, Narayanapanicker A, Ray R, Grieve DJ. 2006. NADPH oxidases in cardiovascular health and disease. Antioxid Redox Signal 8:691–728.
crossref pmid
Choct M, Naylor AJ, Reinke N. 2004. Selenium supplementation affects broiler growth performance, meat yield and feather coverage. Br Poult Sci 45:677–683.
crossref pmid
Christine AZ, Messikommer RE, Caspar W. 2002. Choice feeding of selenium-deficient laying hens affects diet selection, selenium intake and body weight. J Nutr 132:3411–3417.
crossref pmid
Cohen G, Dembiec D, Marcus J. 1970. Measurement of catalase in tissue extract. Anal Biochem 34:30–38.
crossref pmid
Devi GS, Prasad MH, Saraswathi I, Raghu D, Rao DN. 2000. Free radicals antioxidant enzymes and lipid peroxidation in different types of leukemias. Clin Chim Acta 293:53–62.
crossref pmid
Downs KM, Hess JB, Bilgili SF. 2000. Selenium source effect on broiler carcass characteristics, meat quality, and drip loss. J Appl Anim Res 18:61–72.
Finch JM, Turner RJ. 1996. Effects of selenium and vitamin E on the immune responses of domestic animals. Res Vet Sci 60:97–106.
crossref pmid
Fridivich I. 1978. The biology of oxygen radicals. Science 20:87
Georgieva NV, Stoyanchev K, Bozakova N, Jotova I. 2011. Combined effects of muscular dystrophy, ecological stress, and selenium on blood antioxidant status in broiler chickens. Biol Trace Elem Res 142:532–545.
crossref pmid
Hegazy SM, Adachi Y. 2000. Comparison of the effects of dietary selenium, zinc, and selenium and zinc supplementation on growth and immune response between chick groups that were inoculated with Salmonella and aflatoxin or Salmonella. Poult Sci 79:331–335.
crossref pmid
Hoffmann PR. 2007. Mechanisms by which selenium influences immune responses. Arch Immunol Ther Exp 55:289–297.
Ibrahim MT, Eljack BH, Fadlalla IMT. 2011. Selenium supplementation to broiler diets. Anim Sci J 2:12–17.

Koski KG, Marilyn E. 2003. Gastrointestinal nematodes, trace elements, and immunity. J Trace Elem Exp Med 16:237–251.
Krstic B, Jokić Z, Pavlović Z, Zivković D. 2012. Options for the production of selenized chicken meat. Biol Trace Elem Res 146:68–72.
crossref pmid
Kuhn H, Borchert A. 2002. Regulation of enzymatic lipid peroxidation: the interplay of peroxidizing and peroxide reducing enzymes. Free Radic Biol Med 33:154–172.
crossref pmid
Lesson S, Summer JD. 2001. Nutrition of chickens. 4th ednUniversity book; Guelph, Ontario, Canada: p. N1H6N8

Llames C, Fontaine Y. 1994. Determination of amino acids in feeds: collaborative study. J AOAC Int 77:1262–1402.
Marsh JA, Dietert RR, Combs GF. 1981. Influence of dietary selenium and vitamin E on the humoral immune response of the chick. Proceedings of the Society for Experimental Biology and Medicine 166:228–236.
crossref pmid
McKenzie RC, Rafferty TS, Beckett GJ. 1998. Selenium: an essential element for immune function. Immunol Today 19:342–345.
crossref pmid
Niu ZY, Liu FZ, Yan QL, Li WC. 2009. Effects of different levels of vitamin E on growth performance and immune responses of broilers under heat stress. Poult Sci 88:2101–2107.
crossref pmid
Nunes AV, Gozzo AJ, Crus-Silva I, Juliano MA, Viel TA. 2005. Vitamin E prevents cell death induced by mild oxidative stress in chicken skeletal muscle cells. Comp Biochem Physiol C Toxicol Pharmacol 141:225–240.
crossref pmid
Ohkawa Y, Ohishi N, Yagi K. 1979. Assay for lipid peroxides in animal tissue by thiobarbituric acid reaction. Anal Biochem 95:351–358.
crossref pmid
Paglia DE, Valantine WN. 1967. Studies on quantitative characterization of erythrocytes glutathione peroxidase. J Lab Clin Med 79:158–169.

Panda AK, Ramarao SV, Raju MVLN, Chatterjee RN. 2008. Effect of dietary supplementation with vitamins E and C on production performance, immune responses and antioxidant status of White Leghorn layers under tropical summer conditions. Br Poult Sci 49:592–599.
crossref pmid
Papp LV, Lu J, Holmgren A. 2007. From selenium to selenoproteins: synthesis, identity, and their role in human health. Antioxid Redox Signal 9:775–806.
crossref pmid
Payne RL, Southern LL. 2005. Comparison of inorganic and organicselenium sources for broiler. J Poult Sci 84:898–902.
Perić L, Milošević N, Žikić D, Kanački Z, Džinić N, Nollet L, Spring P. 2009. Effect of selenium sources on performance and meat characteristics of broiler chickens. J Appl Poult Res 18:403–409.
Sahin K, Kucuk O. 2003. Heat stress and dietary vitamin supplementation of poultry diets. Nutrition Abstracts and Reviews, Series B 73:41R–50R.
Singh H, Sodhi S, Kaur R. 2006. Effects of dietary supplements of selenium, vitamin E or combinations of the two on antibody responses of broilers. Br Poult Sci 47:714–719.
crossref pmid
Spallholz JE, Martin JL, Gerlach ML, Heinzerling RH. 1973. Enhanced immunoglobulin M and immunoglobulin G antibody titers in mice fed selenium. Infect Immun 8:841–842.
crossref pmid pmc
Tappel A, Tappel A. 2004. Oxidant free radical initiated chain polymerization of protein and other biomolecules and its relationship to diseases. Med Hypothese 63:98–99.
Thompson JN, Scott ML. 1970. Impaired lipid and vitamin E absorption related to atrophy of the pancreas in selenium-deficient chicks. J Nutr 100:797–809.
crossref pmid
Toghyani M, Khodami A, Gheisari AA. 2008. Effect of organic chromium supplementation on meat quality of heat stressed broiler chicken. Am J Anim Sci 3:62–67.
Wiseman H, Halliwell B. 1996. Damage to DNA by reactive oxygen and nitrogen species: role in inflammatory disease and progression to cancer. Biochem J 313:17–29.
crossref pmid pmc
Zhang ZW, Wang QH, Zhang JL, Li S, Wang XL, Xu SW. 2012. Effects of oxidative stress on immunosuppression induced by selenium deficiency in chickens. 10.1007/s12011-012-9439-0

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