Explore

Communities in English

Advertise on Engormix

Enhancing Animal Health and Performance With Ruminally Protected Microencapsulated Antioxidants

Published: October 1, 2019
By: Norbert Chirase, Ph.D. GTX Technologies, Texas A&M University. Winston A. Samuels, Ph.D. Maxx Performance.
Introduction
Economic impact of oxidative stress on the profitability of dairy cows and calves: In the most simplistic terms, the body (humans and animals) could be compared to a medium in which millions of chemical reactions take place with the support of food energy. These reactions are the basis of life without which life will cease to exist. Thus, the body could simply be called the fire of life because oxygen is one of the main substances required by humans and animals to maintain this fire. This fire can neither be allowed to burn out of control nor be extinguished completely. Thus, for a healthy bodily function, an optimum burning of this fire is necessary. Oxidative stress occurs when the generation of reactive metabolites of oxygen (reactive oxygen metabolites/species or free radicals) exceeds their safe detoxification or disposal by the body. In animal production, reactive metabolites of oxygen may occur as a result of physical, biological, and chemical stressors which could result in morbidity, mortality or reduced production. In dairy cows, some important health disorders (retained fetal membranes, udder edema, mastitis) appear to be related to oxidative stress. Also, milk quality and shelf-life could be affected by antioxidants such as vitamins C and E. Pre- and post-weaning periods could be very stressful for dairy calves, thus lowering their immune function and resulting in infection by deadly pathogens.
What are antioxidants?
In the process of the use of oxygen to support life, free radicals or reactive oxygen metabolites (ROM) are formed. Free radicals include singlet oxygen, superoxide, hydrogen peroxide, hydroxyl radical and fatty acid radicals. Free radicals can react with enzymes, cell membranes and DNA damaging them or even causing cell death (process of ageing). Cellular defenses to control or neutralize the harmful effects of free radicals in the body are through 1) Enzymatic neutralizing defenses (Zn/Cu/Mn superoxide dismutase, Fe-catalase, Se-glutathione peroxidase and Se-glutathioneS-transferase), 2) Enzymatic damage repair defenses (lipases, proteases and DNA/RNA repair enzymes), 3) Non-enzymatic defenses (glutathione, uric acid, melatonin, hypotaurine) and 4) Nutrient defenses (carotenoids, ascorbate, tocopherols, tocotrienols, phenols, lycopenes, trace minerals, etc.).
Enhancing Animal Health and Performance With Ruminally Protected Microencapsulated Antioxidants - Image 1
Enhancing Animal Health and Performance With Ruminally Protected Microencapsulated Antioxidants - Image 2
Measurement of oxidative stress in animals:
Research ndicates that when recently weaned calves were purchased at auction barn and transported long distances (e.g. from Tennessee to Texas), the byproducts of lipid peroxidation called malondialdehydes (MDA) increased in the blood (Figure 1) and at the same time their ability to detoxify free radicals as measured by blood total antioxidant capacity (TACA) plummeted (Figure 2). TACA is the total capacity of plasma or tissue to detoxify oxygen radicals. Thus, these calves were predisposed to tissue damage (lung lesions, etc.).
When blood vitamins A and E were measured along with the incidence of bovine respiratory disease (BRD), as their blood antioxidant vitamin concentrations decreased, the incidence of BRD increased (Figures 3 and 4). Ultimately, as the incidence of BRD increased, their performance as measured by average daily gain (ADG) decreased (Figure 5). The lower the vitamin concentration, the more chronically sick they became.
Enhancing Animal Health and Performance With Ruminally Protected Microencapsulated Antioxidants - Image 3
 
Enhancing Animal Health and Performance With Ruminally Protected Microencapsulated Antioxidants - Image 4
Enhancing Animal Health and Performance With Ruminally Protected Microencapsulated Antioxidants - Image 5
 
In another study with calves where blood vitamin C (ascorbic acid) was measured before and after shipment from Arkansas to Texas, calves’ average blood vitamin C concentrations decreased from TN values of 2.67 micro Moles/ liter (uM/L) to 0.16 uM/L (TX), with some calves below detectable levels. This result was very surprising because cattle can synthesize vitamin C.
Thus, marketing and transit stress were either too intense resulting in the depletion of the supply of ascorbic acid or the rumen was not well developed to support vitamin C synthesis. Consequently, calves of this size (dairy and beef) should be supplemented with ruminally protected vitamin C to meet their daily requirements and/or to counter physical, biological and chemical stressors in the production system.
Enhancing Animal Health and Performance With Ruminally Protected Microencapsulated Antioxidants - Image 6
The relationship of blood antioxidants to the immune system was reported in dairy calves raised in commercial calf hutches and indoor metal pens. There was a positive correlation between plasma ascorbate and IgG concentrations in calves housed in metal pens but the relationship was negative for those housed in hutches. Additionally, housing in metal pens decreased plasma cortisol, plasma ascorbate, IgG and specific antibody titers when compared with those housed in commercial hutches.
Calves with respiratory and enteric infections showed decreased plasma concentrations of ascorbic acid. Because calves are not capable of synthesizing endogenous ascorbic acid until 21 days of age, it is inevitable that they should receive ascorbic acid in their diet during this period. Also, the housing type and season of the year (stressors) could prolong the age at which ascorbic acid is synthesized in calves.
Antioxidants and Dairy Health Disorders
  • Clinical mastitis is an expensive disease for the dairy farmer. The total case of management of the disease average $100 to $140 per case.
  • Severity of mastitis increases with a decreased antioxidant capacity.
  • Supplemental vitamin E and Se have been beneficial in reducing prevalence and severity of mastitis and somatic cell counts.
  • Concentration of ascorbic acid is very high in some immune cells and increase as much as 30 fold when stimulated.
  • About 9% of all calvings result in retained fetal membranes (RFM) resulting in $100 to $280/case.
  • Ascorbic acid concentrations are 50% lower in maternal and fetal placental tissues than cows without RFM.
  • At least 300 IU of vitamin E/day is recommended when oxidized flavor in milk is a problem. About 2% of dietary vitamin E is secreted in milk.
Impact of commingling on oxidative stress and BRD:
Dairy calves being raised as replacement heifers or for veal are commonly purchased from several sources. Also, dairy cows are often housed in large groups in a single pen after weaning. Thus, translocation and pathogen distribution through commingling are common practices which could affect the health of cows and calves. Research supporting the effects of commingling stress on BRD was conducted at the Texas A&M University Research Center in Amarillo using calves obtained from two sources (New Mexico and Tennessee) measuring red blood cell (RBC) lysate concentrations of cellular glutathione peroxidase (cGPx), reduced (GSH) and oxidized (GSSG) glutathione and Zn/Cu/Mn superoxide dismutase (SOD). These biomarkers used to assess the incidence of bovine BRD during the receiving period.
Pretransit HB (mg/dL), cGPx (mU) and GSSG (nmol) were lower (P<0.05) in TN steers than NM steers. Thus, distance of translocation was significant in the antioxidant capacity of these calves (Figures 6 and 7). Pretransit cGPx values for TN and commingled calves correlated negatively with incidence of BRD at the feedyard (Figures 8 and 9). As incidence of BRD increased, cGPx concentrations decreased. Also, the lower the blood cGPx and GSSG concentrations of calves, the higher the incidence of BRD (Figures 9 and 10). Thus, with the depletion of the cellular pools of antioxidants, the greater the impact of stressors on the health of the animal.
Enhancing Animal Health and Performance With Ruminally Protected Microencapsulated Antioxidants - Image 7
Enhancing Animal Health and Performance With Ruminally Protected Microencapsulated Antioxidants - Image 8
When dietary antioxidants such as serum free retinol (vitamin A), α- & y-tocopherols (vitamin E) were measured in the blood of these calves, they decreased precipitously from the farm and through the first 28 days at the feedyard. Thus, with the onset of stress, ruminants become morbid and ultimately lose dietary antioxidants due to a reduction in intake and/ or a reduction in their synthesis in the rumen. In the case of calves, antioxidants depletion in the face of stress is even worse because the rumen is not fully developed to support the biosynthesis of ascorbic acid.
Enhancing Animal Health and Performance With Ruminally Protected Microencapsulated Antioxidants - Image 9
In order to compensate for the stress and/ or disease and the reduced or debilitated antioxidant status, dietary supplementation with antioxidants becomes inevitable to sustain life.
In one study, dairy calves fed 0.5 g or 1 g of microencapsulated ascorbic acid pre-weaning gained 15.4% more weight daily when compared with the control calves which did not received supplementary ascorbic acid. The average daily weight gains were also 8.4% higher than the controls with the continued post-weaning ascorbic acid supplementation. The results suggest that microencapsulated ascorbic acid is essential for calves whose antioxidant defense systems are less well developed.  
Dietary sources of antioxidants:
As outlined above, oxidative stress is very common in modern livestock production systems. The economic impact in beef cattle production alone is estimated at billions of dollars due to its relationship to BRD. In other production systems such as dairy, swine and poultry, there are similar economic effects, ultimately affecting the profitability of the overall livestock industry. Who would ever believe that feeder calves originating from lush green native pastures of calf producing areas (TN, KY, AR and NM) would be deficient in serum free retinol resulting from auction barn sale and transit stress?
Enhancing Animal Health and Performance With Ruminally Protected Microencapsulated Antioxidants - Image 10
Who would ever believe that cattle unlike humans that can synthesize ascorbic acid would not have detectable levels of this key antioxidant in their blood? 
Oxidative Stress and the transition Dairy Cow:
Classically, the transition period (defined as late pregnancy to early lactation) spans 21 days prepartum to 21 days postpartum. However, this period could be greater because of biological, chemical and environmental stressors preponderant at the dairy farm. A reduction in nutrient intake in the phase of dramatic increase in nutrient requirements is a common characteristic of this period. Thus, the risk of metabolic disorders increases with decreasing profits. Other losses associated with antibiotic treatment and delayed breeding may occur. However, by far the most economically important metabolic disorders that drain profits are ketosis, milk fever, displaced abomasums, retained placentas (or fetal membranes), mastitis, metritis and dystocia, all occurring during this critical period of the lactation cycle. Some of these disorders occur because of a depression in the immune system. Plasma alpha tocopherol (vitamin E) concentrations have been reported to be depressed by as much as 47% at calving. When high levels (1,000 IU per head daily) of vitamin E were fed for 21 days prior to calving, reduced retained placentas was observed. In the phase of decreasing circulating levels of progesterone and glucocorticoids, dietary vitamin E seems to enhance the immune system. Thus, oxidative stress during the transition period could be the transition dairy cow. To remediate against these problems, a balanced antioxidant nutrition is recommended during this period. 
Two major antioxidant vitamins manufactured by Maxx Performance (Roanoke, VA) are available to replenish the antioxidant status of ruminants. Microencapsulated Vitamin C is a stabilized vitamin C that when used as a supplement in animal feed is temperature and low pH resistant and will escape ruminal microbial degradation and become biologically available to all ruminants and nonruminants.
By microencapsulation, ascorbate is also physically protected from air, light and metals, thus maintaining its potency (raw supplements are exposed to destruction before they’re needed). Microencapsulated Vitamin C is the most potent form of ascorbic acid which is a powerful reducing agent (electron donor) and participates in intracellular and extracellular quenching of reactive oxidants, recycling of vitamin E (electron transfer to oxidized tocopherols and tocotrienols), participates (co-factor) in 8 major and essential enzymatic reactions, prevention of LDL oxidation, and promotes iron absorption in the gastrointestinal tract. Microencapsulated Vitamin C is free flowing and contains 70% ascorbic acid and can be manufactured in various particle size ranges for compounding with different feeds. Packaging is in 50-pound, poly-lined recyclable cartons that can be stacked in a pallet (4 layers of 10 cartons) for shipping.
Coated Vitamin E is also a microencapsulated vitamin E (a-tocopherol acetate) that when used as a supplement in animal feed is temperature and pH resistant and will escape ruminal microbial degradation and become biologically available to all ruminants and nonruminants. The major antioxidant function of vitamin E (tocopherols and tocotrienols) is to prevent lipid peroxidation. In the cell membrane, it’s been estimated that there is 1 tocopherol molecule for every 1000 lipid molecules. With its phytyl tail buried in the membrane and its chroman ring on the surface, the tocopherol molecule acts as an antioxidant and is regenerated from its oxidized form by interacting with other antioxidants, particularly vitamin C; thus, the two vitamins synergizing to produce maximum biological response during stress. In recognition of this synergy, Maxx Performance has an expansive microencapsulation technology platform for producing Vitamin C and Vitamin E together in a compact single spherical combination particle for ease of handling.
Enhancing Animal Health and Performance With Ruminally Protected Microencapsulated Antioxidants - Image 11
In extreme stressful situation, a very rapid detoxification is needed to restore health and maintain production. Microencapsulated Vitamin CE combination comes in 50-pound, poly-lined recyclable cartons that can be stacked in a pallet (4 layers of 10 cartons) for shipping.
Microencapsulated coated Lysineis a ruminally protected form of the essential amino acid lysine. Cattle do require essential amino acids just like nonruminants, especially if deficiency is created by the stress of production and/or the rumen is not well developed to provide microbial sources of lysine. With the shift away from using animal protein sources in animal production, nutritionists are looking for cost effective sources of essential amino acids, especially lysine to meet animal requirements. Microencapsulated Lysine by Maxx Performance is a stabilized free flowing lysine and provides the most effective way to supplement ruminants directly without the interference of ruminal microbes. Lysine is required for protein synthesis without which the performance (ADG, milk, eggs, reproduction) of livestock is reduced. Maxx Performance rumen protected Lysine comes in 50-pound, poly-lined recyclable cartons that can be stacked in a pallet (4 layers of 10 cartons) for shipping. 

Blair, L and K.A. Cummins. 1984. Effect of dietary ascorbic acid on blood immunoglobulin concentration in dairy calves. J. Dairy Sci. 67(Suppl. 1):138. (Abstr).

Bortree, A.L, C.F. Huffman, and C.W. Duncan. 1942. Normal variations in the amount of ascorbic acid in the blood of dairy cattle. J. Dairy Sci. 25:983.

Bouda, J., P. Jagos, K. Dvorak, and J. Ondrova. 1980. Vitamin E and C in the blood plasma of cows and their calves fed from buckets. Acta Vet. Bmo. 49:53.

Cappa, V. 1958. Destruction of vitamin C by the bacterial flora of the rumen. Riv. Zootec. 31:199.

Chatterjee, I.B. 1978. Ascorbic Acid Metabolism. World Rev. Nutr. Diet. 30:69

Chatterjee, I.B, A.K. Majumder, B.K. Nandi, and N. Subramanian. 1975. Synthesis and some major function of vitamin C in animals. Ann. N.Y. Acad. Sci. 258-24.

Chirase , N. K, L. W. Greene, C. W. Purdy, R. W. Loan, R. E. Briggs, and L. R. McDowell. 2001. Effect of environmental stressors on ADG, serum retinal and y-tocopherol concentrations, and incidence of bovine respiratory disease of feeder steers. J. Dairy Sci. (Suppl. 1):84/J. Anim. Sci. (Suppl. 1):79/ Poultry Sci. (Suppl. 1):80/Proceedings of the 54th Annual Reciprocal Meat Conference. Vol II:188 (abstr.).

Chirase , N. K, L. W. Greene, C. W. Purdy, R. W. Loan, D. R. George, and J. Avampato. 2001. Influence of dietary antioxidant vitamins on performance of feeder steers exposed to simulated feedyard manure dust. J. Dairy Sci. (Suppl. 1):84/J. Anim. Sci. (Suppl. 1):79/ Poultry Sci. (Suppl. 1):80/Proceedings of the 54th Annual Reciprocal Meat Conference. Vol II: 188 (abstr.).

McBride, K. W., L. W. Greene, N. K. Chirase, E. B. Kegley and N. A. Cole. 2001. The effects of ethoxyquin on performance and antioxidant status of feedlot steers. J. Dairy Sci. (Suppl. 1):84/J. Anim. Sci. (Suppl. 1):79/Poultry Sci. (Suppl. 1):80/Proceedings of the 54th Annual Reciprocal Meat Conference. Vol II:285 (abstr.).

Chirase, N. K, C. W. Purdy, L. W. Greene and J. Avampato. 2001. Effect of feedyard manure dust on performance and health of young Spanish goats. Written for presentation at the 2001 American Society of Agricultural Engineers (ASAE) Annual International Meetings sponsored by ASAE, Sacramento Convention Center, Sacramento, CA, USA, July 30 – August 1, 2001.

Chirase , N. K, C. W. Purdy, R. W. Loan, R. Briggs, G. Duff, J. Avampato and D. Murray. 2002. Influence of transportation stress and prophylactic antibiotic on oxidative stress biomarker status and incidence of bovine respiratory disease of feeder cattle. J. Dairy Sci. (Suppl. 1): 85/J. Anim. Sci. (Suppl. 1): 80: 86 (abstr.).

Chirase , N. K, C. W. Purdy, R. W. Loan, R. Briggs, G. Duff and J. Avampato. 2002. Effect of environmental stressors and prophylactic antibiotic on serum antioxidant concentrations and incidence of bovine respiratory disease of feeder cattle. J. Dairy Sci. (Suppl. 1): 85/J. Anim. Sci. (Suppl. 1): 80: 86 (abstr.).

Chirase , N. K, C. W. Purdy, R. W. Loan, R. Briggs, G. Duff and J. Avampato. 2002. Effect of environmental stressors and prophylactic antibiotic on performance and incidence of bovine respiratory disease of feeder cattle. J. Dairy Sci. (Suppl. 1): 85/J. Anim. Sci. (Suppl. 1): 80: 183 (abstr.).

Chirase, N. K., C. W. Purdy, and J. M. Avampato. 2004. Effect of simulated ambient particulate matter exposure on performance, rectal temperature and leukocytosis of young Spanish goats with or without tilmicosin phosphate. J. Anim. Sci. 82:1219-1226.

Chirase, N. K, L. Wayne Greene, Charles W. Purdy, Raymond W. Loan, Brent W. Auvermann, David B. Parker, Earl F. Walborg, Jr., Donald E. Stevenson, Yong Xu and James E. Klaunig. 2004. The effect of transport stress on respiratory disease, serum antioxidant status and lipoperoxidation levels in beef cattle. American J. Vet. Res. Vol. 65 (No. 60).

Cummins, K.A. and C.J. Brunner. 1987. Effect of orally administered ascorbate and colostrums deprivation on immune response of calves. J. Dairy. Sci. 70 (Suppl. 1):204(Abstr.).

Cummins, K.A. snd C.J. Brunner. 1989. Dietary ascorbic acid and immune response in dairy calves. J. Dairy Sci. 72:129. Cummins, K.A. snd C.J. Brunner. 1989. Factors affecting plasma ascorbate and dehydroascorbate concentration in dairy calves. J. Dairy Sci. 72(Suppl. 1):501 (Abstr.).

Cummins, K.A. snd C.J. Brunner. 1990. Effect of calf housing on plasma ascorbate and endocrine and immune functions.

Dodsinska, E., Z. Sova, V. Kopak, and M. Trhon. 1981. Relations among glycerniam ascorbernia and weight gains in calves in a large capacity calfhouse. Vet. Med. Praha 26:203.

Dobinsky, O., L. Itze, and M. Pospisil. 1979. Vitamin C levels in the early post-natal period in calves and their mothers. Vet. Med. Praha 24:385. Duncan, C.W. 1944. Studies in the influence if ascorbic acid in calves with scurvy. J. Dairy Sci. 27:636.

Dvorak, M. 1964. Blood serum L-ascorbic acid in calves fed with 2% fat. Vet. Med. Praha 9:471.

Dvork, M. 1966. Blood serum ascorbic acid in cows and bulls on winter and summer nutrition. Vet. Med. Praha 11:73.

Goff, J. P., and J. R. Stabel. 1990. Alphatocopherol and zinc concentrations during the periparturient period: Effect of milk fever. 73:3195-3199. Goff, J. P., and R. L. Horst. 1997. Effects of addition of potassium or sodium, but not calcium, to prepartum rations on milk fever in dairy cows. J. Dairy Sci. 80:176-186.

Gosse, P.T. 1938. Effects of vitamin C intake on depletion time in calves. J. Dairy Sci. 20:666.

Haag, W. 1987. Vitamin C content in blood plasma and leukocytes of cattle. Tieraerzti. Umsch. 42:956.

Haag, W. 1987. Vitamin C in cattle: Occurrence and effects. Deutsche Tierar. Wochenschrift. 94:181.

Hibbs, J.W. and W.D. Pounder. 1948. The influence of the ration and early rumen development on the changes in the plasma carotenoids, vitamin A and ascorbic acid of young dairy calves. J. Dairy Sci. 31:1055.

Hidiroglou, M., M. Ivan, and J.R. Lessard. 1977. Effects of ration and inside versus outside housing an plasma levels of ascorbic acid, lactic acid, glucose and cholesterol in Hereford steers wintered under practical conditions. Can. J. Anim. Sci. 57:519.

Itze, L. 1984. Ascorbic acid metabolism in ruminants. Pages 120-130. In Proceedings Ascorbic Acid in Domestic Animal Workshop. Royal Danish Agric. Socio. Copenhagen, 1984.

Itzeova, V. 1984. Ascorbic acid and immunoglobulin in serum of calves in relation to different types of colostral nutrition. Pages 139-147. In: Proceedings of Ascorbic Acid in Domestic Animals Workshop. Royal Danish Agric. Soc., Copenhagen, 1984.

Jagos, P., J. Bounda, and R. Dvorak. 1977. The ascorbic acid levels in case of bronchopneumonia of calves. Vet. Med. Praha 22:133.

Kitabchi, A.E. and W.H. Wesr. 1975. Effect of steroidogenesis on ascorbic content and uptake in isolated adrenal cells. Ann. N.Y. Acad. Sci. 258:422.

Knight, C.A., R.A. Dutcher, N.B. Cuerrant, and S.I. Bechdel.1941. Utilization and excretion of ascorbic acid in the dairy cow. J. Dairy Sci. 24:567.

Kolb, E., M. Wahren, G. Dobeleit, and G. Grundel. 1989. The content of ascorbic acids in different tissues in cattle, normally-developed piglets, splay-legged piglets, adult swine, and dogs. Arch. Exp. Vet. 43:327.

Lundquist, N.S. and P.H. Phillips. 1942. Age related studies on ascorbic acid metabolism in animals. J. Dairy Sci. 25:586.

Lundquist, N.S. and P.H. Phillips. 1943. Certain dietary factors essential for the growing calf. J. Dairy Sci. 26:1023.

Muller, Z. 1960. Vitamins in Animal Production. SVPL. 462 pp.

Palludan, B. and I. Wegger. 1984. Plasma ascorbic acid in calves. Pages 131-138. In:Proceedings of Ascorbic Acid on Domestic Animal Workshop. Royal Danish Agric. Soc., Copenhagen. 1984.

Phillips, P.H., H.A. Lardy, P.D. Boyer, and G.M. Werner. 1941. The relationship of ascorbic acid to reproduction in the cow. J. Dairy Sci. 24:153.

Rassmussen, R., N.B. Guerrant, A.O. Show, R.C. Welch, and S.I. Bechdel. 1936. The effects of breed characteristics and stages of lactation on the vitamin C (ascorbic acid) content of cow’s milk. J. Nutr. 11:425.

Riddell, W.H. and C.H. Whitnah. 1938. Vitamin C. Metabolism in the dairy cow. J. Dariy Sci. 21:121 (Abstr).

Riddell, W.H. and C.H. Whitnah, J.S. Hughes, and H.F. Leinhardt. 1936. Influence of the ration on the Vit. C. content of milk. J. Nutr. 11:47.

Robinson, J.A., B.A. Gulick, and R.E. Hodges, and B.W. Glad. 1979. Comparative studies of whole and plasma ascorbic acid levels in some species of animals. Fed. Proc. 38:556 (Abstr.).

Roth, J.A. and M.L. Kaeberle. 1985. In vivo effect of ascorbic acid on neutrophil function in healthy and dexamethasone-treated cattle. Am. J. Vet. Res. 46:2434.

Salageanu, G., D. Curca, I. Ursa, and A. Batrinu. 1971. Hypovitaminosis C in newborn calves with enteropathies. Rev. Zootech. Med. Vet. 21:57.

Sato, P.H. and S. Udenfriend. 1978. Scurvyprone animals including man, monkey, and guinea pig do not express the gene for gulonolactone oxidase. Arch. Biochem. Biophys. 187:158.

Schreiber, M., P. Novy, and S. Trojan. 1989. The effect of acute and chronic hypoxia on the ascorbic acid levels in various areas if the brain, liver, adrenal glands, and in boil. Fluids in 18-d-old rats. Sb. Lek. 91:129.

Scott, D.W. 1983. Vitamin C responsive dermatosis in calves Pract. Vet. 3:10.

Scott, M.L. 1975. Envirnmental influences in ascorbic acid requirements in animals. Ann. N.Y. Acad. Sci. 358:151.

Sheahan, M.M. 1947. The ascorbic acid content of the blood serum of farm animals. J. Comp. Pathol. 57:28.

Smimov, A.N. 1962. (Caroten and ascorbic acid levels related to the growth and health status). Veterinarija 39:40.

Soldatenkov, P.F. and N.M. Suganova. 1966. On the vitamin C exchange in cattle. Seiskochoz Biol. 1:446.

Tillotson, J.A. and E.L. McGowan. 1981. the relationship of urinary ascorbic metabolism to specific levels of ascorbic ssupplementation on the monkey. Am. J. Clin. Nutr. 34:2405.

Vavrich, M. 1945. Importance of vitamin C in calves and cows. J. Dairy. Sci. 28:759.

Watts, J. 1950. Studies on vitamin A and C in bovines. J. Comp. Pathol. Ther. 60:283.

Wegger, I. and J. Moustgaard. 1982. Age variation in plasma ascorbic acid in calves (Danish En. Summary). Annu. Rep. Sterility Res. Inst., Royal Vet. and Agric. Univ., Copenhagen 25:16.

Related topics:
Authors:
Winston Samuels
Maxx Performance
Recommend
Comment
Share
rimdha
29 de septiembre de 2020

Do you have an idea if this can be an admitted technique?

"30 g orange peel essential oil + 970 g zeolite were mixed
and then added to basal diet to obtain 300 ppm of essential oil concentration" (published article)

I'm interested in protecting EO for small scale to conduct experimental trials. without an efficient stabilization protocol, in vivo assays are just impossible!

Recommend
Reply
Courtney Samuels
Maxx Performance
25 de noviembre de 2019
The power of microencapsulation!
Recommend
Reply
AVR KUMAR
21 de octubre de 2019
Shall we combine maize flour with locally available vitamin compounds
Recommend
Reply
Profile picture
Would you like to discuss another topic? Create a new post to engage with experts in the community.
Featured users in Dairy Cattle
Jim Quigley
Jim Quigley
Cargill
Technical Lead - Calf & Heifer at Cargill
United States
Pietro Celi
Pietro Celi
DSM-Firmenich
DSM-Firmenich
United States
Mauricio Grierson
Mauricio Grierson
MSD - Merck Animal Health
MSD - Merck Animal Health
United States
Join Engormix and be part of the largest agribusiness social network in the world.