What are oxidizing substances or ROS (Reactive Oxygen Species)?

In chemistry it is said that a chemical element undergoes oxidation when it undergoes an electron subtraction, which translates into an increase in its oxidation number. This subtraction of electrons can take place by another element, which thus undergoes the complementary reduction process. Most oxidation reactions involve the development of energy in the form of heat and electricity. Substances that have the ability to oxidize other substances are known as oxidizing agents or ROS.

They subtract electrons from other substances and in practice accept electrons. Oxidizers are generally chemical substances that possess elements with a high number of oxidation, for example hydrogen peroxide, permanganate or highly electronegative substances such as oxygen (eg: air), flower, chlorine (eg: sea salt) or bromine, capable of removing one or more electrons from other substances.

Oxidation

Simple classic examples: Piece of oxidized metal (corroded) – Corrosion

Oxidation is a chemical reaction that transfers electrons from a substance to an oxidizer.
Oxidation reactions produce free radicals or ROS, which are responsible for initiating a chain reaction that damages cells. Antioxidants terminate these chain reactions by intervening on intermediate radicals and inhibiting other oxidation reactions by oxidizing themselves.

Oxidative stress

Oxidative stress is a pathological condition caused by the breakdown of physiological equilibrium, in a living organism (vegetable, animal or human), between the production and elimination, by antioxidant defense systems from oxidizing substances.
All life forms maintain an “antioxidant reducing environment” (antioxidant stock) within their cells. In the REDOX cellular environment (with the term redox or redox from the English REDduction, reduction and OXidation, oxidation) all those chemical reactions take place in which the oxidation number of the atoms changes (ie all the reactions in which there is an exchange of electrons from one chemical structure to another) it is preserved by enzymes that maintain the reduced state through a constant input of metabolic energy.
Possible alterations of the normal REDOX state can have toxic effects for the production of peroxides and free radicals that damage all the components of the cell, including proteins, fats and DNA intervening negatively in the systems of self-defense (immunodepression) and in the health of the organis.

Cellular oxidative stress

Oxidative stress, on the part of free radicals and how, these oxidative processes, can cause significant oxidation at the level of the cell membrane and destroy DNA. Today it is possible to evaluate them by means of tests that help us assess the state of health of the organism , the inflammatory state and the onset of some diseases (eg: in humans pathologies such as diabetes, Alzheimer’s and cardiovascular diseases, but also in animals as in pigs with the onset of “very aggressive viral and bacterial forms that are not very sensitive to normal drugs, such as PRRS, etc … or even, not less important, lack of productive and qualitative performances).
Today it is possible to measure both the production of free radicals and the body’s ability to react to oxidative stress through the antioxidant barrier that includes both endogenous antioxidants (complex enzyme systems) and exogenous ones (ie those that are taken through nutrition), and also antioxidant power of a particular functional food (KRL test on red blood cells).

Classic example “on the apple” of damage from free radicals at the cellular level

Definition of antioxidants

Antioxidants are natural and non-natural chemical substances (molecules, ions, radicals) or physical agents that slow down or prevent the oxidation of other substances as a result. The antioxidants are chemically defined of involve as reducing agents (such as thiols and polyphenols) as the chemicals involved in to reactions in thr oxide-reducing. Although oxidation reactions are vital for life, they can be just as harmful; therefore, both plants and animals maintain multiple types of antioxidants as complex self-defense systems.

Antioxidants can be ….

• Primary:
  1) When they prevent the production of “species” of radicals
  2) When “grappling ” on the transition metals
• Secondary: when they react with the newly formed radicals and convert them into non-reactive forms by interrupting the chain reaction and therefore can be:

1. Endogenus: quando sono sintetizzati dall’organismo stesso( enzimatici cellulari) ed a seconda della loro azione posso essere
   a) 1) Enzyme type cellular, as:
   – SOD (superoxide dismutase), catalase and glutathio-peroxidase (it is the main cellular antioxidant that maintains low O2 level and works in conjunction with Catalase and Glutathione Peroxidase (GSH-Px —-> Vit E + Se) it is the main “detoxifier” of the cells:

    

   
   – 2. The Catalase (CAT): 2 H2 O2 ——> 2 H2O + O2
   b) Type Protein as SH and metallic sequestering agents (Fe, Cu,)

2. Exsogenus:
   – Vitaminics: Vitamin C and Vitamin E and Carotenoids (as provitamin A)
   – Polyphenols and Bio-flavonoids

How do antioxidants work?

The oxidation process is a chemical reaction that transfers electrons from a substance to an oxidizer

The nitrogen metabolism in dairy cows:
(by M. Wattiaux – Babcock Institute for International Dairy Research and Development University of Wisconsin – 2014)

The nitrogen metabolism in dairy cows:

The ruminal pH change caused by a sudden and / or sharp increase in rumen soluble nitrogen (protein imbalance), resulting in:

• one excessive ingestion of highly soluble fresh protein fodder (ex: excessive doses of green pasture rich in soluble nitrogen such as alfalfa and / or clover, etc …)
• the use of high doses of silage with a high content of NH3 in free form in the ration, etc … causes both a soluble nitrogen poisoning in the rumen which can also be followed by an acute alkalosis (but only on some subjects) and more as one increase in ammoniacal nitrogen at a ruminal habitat followed by one metabolic level of NH3 (subacute form) which then, in practice, is also the most damaging for economic purposes as it covers the whole herd

Effects on animal health and production:

This situation at rumen level creates the ideal conditions for the development of the Allisonella histaminiformans, a ubiquitous microorganism of the rumen producing histamine that results in:

• the immediate inflammation of the rumen papillaes (due to increased circulating cytokines) and consequent reduction in the assimilation of AGVs (Volatile Fatty Acids) followed by the activation of diseases affecting:
  • udder (increase in the infimmatory state in the breast and consequently more CSS and mastitis)
  • feet (formation of thrombus at amatic level >> interdigital phlegmon >> laminitis)
  • ovaries (ovarian cysts)
• in some animals the acute form (acute alkalosis) may also occur with diseases affecting:
  • liver (hepatic steatosis)
  • of the kidneys (nephritis)
    and in severe forms
  • CNS (neuroplegic symptoms with ataxia, impaired gait etc … and in some cases coma and death of subject Struck)

Actions to be taken on the ration for the subacute forms to improve the health, reproduction and production of cows:

• Elimination and / or reduction of the toxic nitrogen food source ( green grass, grass silage, urea, etc …) and
  add the following mix to the ration
• mix of sodium propionate 100 g / head / day + 20 g. / head/ days of Micronil ® (ProbioactiFAP®) + ANTIGRIP FEED (NUTRIVIT-COFATHIM phytotherapic with an anti-inflammatory action ) 50g./head/days This mix must be administered until the end of the use of the “toxic” ( ex: grass silage ) feed source in the diet and continue for at least another 10 days and continue for at least another 10 days.

BIBLIOGRAPHICAL REFERENCES
– Anon. Third External Review Draft of Air Quality Criteria for Particulate Matter (April, 2002). Volume I, II. EPA. United States Department of Environmental Protection Agency. www.epa
– Bach A., Calsamiglia, S. and Stern, M.D. 2005. Nitrogen Metabolism in the Rumen J. Dairy Sci., 88: 9 – 21 Baker, L.D., J.D. Ferguson, and C.F. Ramberg. Kinetic analysis for urea transport from plasma to milk in dairy cows. J. Dairy Sci. 75 (Supplement 1):181, 1992.
– Baker, JL, 2001. Limitations of improved nitrogen management to reduced nitrate leaching and increase use efficiency. Optimizing Nitrogen Management in Food andEnergy Production and Environmental Protection: Proceedings of the 2 nd International Nitrogen Conference on Science and Policy. The Scientific World 1(S2), 1016.
– Cowling, E., J. Galloway, C. Furiness, M. Barber, T. Bresser, K. Cassman, J.W. Erisman, R.Haeuber, B. Howarth, J. Melillo, W. Moomaw, A. Mosier, K. Sanders, S. Seitzinger, S.Smeulders, R. Socolow, D. Walters, F. West, and Z. Zhu. 2001. Optimizing nitrogen management in food and energy production and environmental protection: Summary Statement from the Second International Nitrogen Conference. TheScientificWorld 1(S2): 19. DePeters, E.J. and J.D. Ferguson. 1992. Nonprotein nitrogen and protein distribution in the milk of cows. J. Dairy Sci. 75:31923209.
– Dou, Z., D.T. Galligan, C.F. Ramberg, Jr., C. Meadows, and J.D. Ferguson. 2001. A survey of dairy farming in Pennsylvania: Nutrient management practices and implications. J. Dairy Sci. 84:966973.
– Ferguson, J.D., Z. Dou, and C.F. Ramberg, Jr. 2001. An assessment of ammonia emissions from dairy facilities in Pennsylvania. TheScientificWorld 1(S2): 348355. Erickson, G.E. and T.J. Klopfenstein. 2001. Nutritional methods to decrease N losses from opendirt feedlots in Nebraska. TheScientificWorld 1(S2): 836843.
– Ganong, W.F. Review of Medical Physiology. Nineteenth edition . Co 1999. Appleton and Lange a Simon & Schuster Company. Stamford, Ct. 069120041.
– Hof, G., M.D. Vervoorn, P.L. Lenaers, and S. Tamminga. 1997. Milk urea nitrogen as a tool to monitor the protein nutrition of dairy cows. J. Dairy Sci. 80:33333340.
– Huhtanen, P. 1998. Supply of nutrients and productive responses in dairy cows given diets based on restrictively fermented silage. Agric. Food Sci. Finl. 7:219–250
– Jarvis, S.C., D.J. Hatch and D.H. Roberts. 1989a. The effects of grassland management on nitrogen losses from grazed swards through ammonia volatilization; the relationship to excretal N returns from cattle. J. agric. Sci. Camb. 112:205216.
– Jarvis, S.C., D.J. Hatch and D.R. Lockyer. 1989b. Ammonia fluxes from grazed grassland: annual losses from cattle production systems and their relation to nitrogen inputs. J. agric. Sci. Camb.113:99108.
– Jonker, J.S., R.A. Kohn, and R.A. Erdman. 1998. Using milk urea nitrogen to predict nitrogen excretion and utilization efficiency in lactating dairy cows. J. Dairy Sci. 81:26812692.Muck, R.E. and B.K. Richards. 1983. Losses of manurial N in freestall barns. Agric. Wastes 7:6579.
– Muck, R.E. 1982. Urease activity in bovine feces. J. Dairy Sci. 65:21572163.
– Muck, R.E. and F.G. Herndon. 1985. Hydrated lime to reduce manorial nitrogen losses in dairy barns. Transactions of ASAE 28:201208.
– NRC. 2001. Nutrient Requirements of Dairy Cattle. Seventh Revised Edition. National Academy Press. Washington D.C. NRC. 1996. Nutrient Requirements of Beef Cattle. Seventh Revised Edition. National AcademyPress. Washington D.C.
– Roseler, D.K., J.D. Ferguson, C.J. Sniffen and J. Herrema. 1993. Dietary protein degradability effects on plasma and milk urea nitrogen and milk nonprotein nitrogen in Holstein cows. J. Dairy Sci. 76:525534.
– Scholefield, D., D.R. Lockyer, D.C. Whitehead, and K.C. Tyson. 1991. A model to predict transformations and losses of nitrogen in UK pastures grazed by beef cattle. Plant and Soil132:165171.
– Smits, M.C.J., H. Valk, A. Elzing, and A. Keen. 1995. Effect of protein nutrition on ammonia emission from a cubicle house for dairy cattle. Live. Prod. Sci. 44:147156.
– Voorburg, J.H. and W. Kroodsman. 1992. Volatile emissions of housing systems for cattle.Livestock Prod. Sci. 31:5770.
– Wattiaux , M.A – Protein Metabolism in Dairy Cows – Babcock Institute for International Dairy Research and Development – University of Wisconsin-Madison -2014
– Wilkerson, V.A., D.R. Mertens, and D.P. Casper. 1997. Prediction of excretion of manure and nitrogen by Holstein dairy cattle. J. Dairy Sci. 80:31933204.
– Van Horn HH. 1991;Managing Dairy Manure Resources to aviod Environmental pollution. J Dairy Sci 77:2008-1994.
– Van Horn HH. Balancing nutrients, manure use reduces pollution. Feedstuffs. The Miller Publishing Co. 1992; 64(Oct. 26, 1992). 11-23. Minnetonka, MN.
– Vanfaassen HG, Lebbink G. 1994;Organic matter and nitrogen dynamics in conventional versus integrated arable farming. Agr Ecosyst Environ 51:209-26.
– Vanhorn HH, Wilkie AC, Powers WJ, Nordstedt RA. 1994;Components of Dairy Manure Management Systems. J Dairy Sci 77:2008-30. Webb J, Archer JR. ; Dewi IA, Axford RFE, Marai IFM, Omed H, editors.Pollution in Livestock Production Systems. Oxon, UK: CAB International, 1994; 11,
– Pollution of Soils and Watercourses by Wastes from Livestock Production Systems. p. 189-204.
– Young CE, Crowder BM, Shortle JS, Alwang JR. 1985;Nutrient Management on Dairy Farms in Southestern Pennsylvania. J Soil Water Conserv 40:443-445.

Natural sources of Vitamin A
Fish liver oil (halibut, cod, salmon, etc.) has always been considered, universally by all researchers, scientists, doctors and nutritionists, as the best existing source of natural Vitamin A . One of the richest fish of theis vitamin, which lives in the North Pacific (Alaska) within the Arctic circle is the Halibut belonging to the Hippoglossus hippoglossus varieties.

How is processed?
After extraction, the oil is processed to obtain different types, more or less purified and concentrated, destined respectively for the pharmaceutical, cosmetic and zootechnical industries. The quality of the oil depends not only on Retinol or Vitamin A but also on the degree and technique of refining, the degree of rancidity, the degree of purity and its pollution and contamination index, both bacterial and of inorganic residues, with particular reference to heavy metals (mercury, lead, cadmium, etc …), and to hydrocarbons (oil and derivatives). Therefore, it requires careful processing by suitably equipped industries and able to guarantee excellent quality that is constant over time at acceptable prices.

Bibliographic source:
Verage values in Retinol (Vitamin A) e cholecalciferol (vitamin D3) in the liver of some marine fish (Table 2.4 – 3.2, Russell Lee – Mc Dowell “Vitamin in Animal Nutrition” Acc.Press, California, 1989.

Natural Vitamin A or Retinol, naturally contained in this type of oil, although apparently similar to that produced synthetically by the chemical industry, is profoundly different and to and say affirm , as many technicians do in the zootechnical field, that Vitamin A obtained by chemical synthesis it has the same biological value as the natural one (ie biologically active), it is an obvious gross error. They are two distinct products that have nothing in common but the denomination, in fact they have one:

1. similar but not equal molecular structure
2. different chemical composition
3. different melting point
4. different molecular weight

It was the prof. McCollum in 1926 at the Experimental Agricultural Station in Madison (Wisconsin – USA) who pointed out that the vital factor contained in the fish liver oil of the “Arctic” (improved spermatogenesis in boars)seas was a fat-soluble substance (chemically belonging to the amine group) and since then it was assumed that vital factors of this kind contained in food were more than one, they called it seen Vitamin A, since it was the first. Later the same researchers discovered that the grass of some pigmented plants such as alfalf and carrots and many other plants, had similar properties. Thus they came to the conclusion that even in the plant world there was a vital food factor of this type, this time water soluble. Only later, with the evolution of biochemical studies, was it possible to state with certainty the existence of two sources of this vitamin.
The first is a real vitamin called Retinol of exclusive animal origin and the second a provitamin called water-soluble β-Carotene of exclusive vegetable origin, which once taken by the animal is transformed into Retinol or Vitamin A in intestinal cells:

Biochemical differences between Natural Retinol and synthetic Vitamin A
The naturally occurring Retinol is in two chemically similar but not identical forms called A1 and present at 95% in marine fish oil and A2 or 3-dehydroretinol present in the same 5% oil. The form A1 which is the only synthetically reproduced. Retinol occurs naturally in two forms called “vitamers”
1) Retinal ‘all trans’
2) Retinal ‘11 cis ’
The form A2 or 3-dehydroretinol is not reproducible and is distinguished by the presence between the C3 and C4 of a double bond = unsaturated. Vitamer A1 is undoubtedly the most functional, while Vitamer A2 is not exactly known for its function other than acting as a synergist of A1 and cannot be reproduced synthetically.
This partly explains why dosages of natural Vitamin A or Retinol, all in all quite modest, have given physiological responses much higher than those normally obtained at high dosages with synthetic ones and why the latter is not at all toxic.

GABALDO G. (1), DEPALMA A. (2), FUSARI A. (3), PIZZICARA M. (1), TINELLI S. (2) , UBALDI A. (3)

(1) TE.CO.S. srl – Verona – Italy; (2) Veterinary Pratictioner – Italy ; (3)Dipartimento di Salute Animale, Università degli Studi di Parma – Italia

INTRODUCTION

Polyunsatured Fatty Acid or PUFAs must be introduced compulsorily with the diet. (So called Essential Fatty Acids). Numerosus articles have shown that introducing Omega 6 or Omega 3 in the diet of dairy cows, mainly in risk period as « Transition Period », Improve both reproductive and immune status of dairy cows No trials were performed with an association of those family of PUFAs, neither with a stimulation of Rumen’s flora.

THE DHA IN THE RUMEN

It was found in vitro and in vivo that DHA-enriched micro algae have an inhibitory effect on rumen biohydrogenation of polyunsaturated fatty acids resulting in the accumulation of several hydrogenation intermediates such as conjugated linoleic acid (CLA c9t11), well known for its anticarcinogenic and antiartherogenic effects, and vaccenic acid (C18:1 t11), the precursor of CLA in the mammary gland. Recently Belgian and Dutch researchers (Boeckaert – Vlaeminck and coll – 2007) have demonstrated the accumulation of biohydrogenation intermediates was associated with the disappearance of some rumen ciliates.

IPOTESI DEL RUOLO DEL FAP® nel metabolismo del DHA

LeVif ® : STEMMED FROM A NATURAL TECHNOLOGIC INDUSTRIAL PROCESS, WHICH ENHANCE THE VALUE OF THE GRAIN BY GERMINATION AND LACTIC FERMENTATION

LeVif ® : SYMBIOTIC (probiotic+prebiotic) action on ruminal protozoan population

Compensation  for the inhibitory  effect of  the ruminal protozoan population on D H A

More DHA  available in the metabolism

DISCUSSION

1. The increase of a part of saturated fatty acids (C12-C14-C16) inthe treated group is balanced by the decrease of C18 (stearic acid)
2. At the end the level of saturated fatty acid in the milk is healthier for the human nutrition
3. The most interesting part of unsaturated fatty acids for the human nutrition is:

           => CLA: + 109,34%  /   => EPA + DHA = + 19,48%

With a decrease of EPA (-57%) but a very important increase of DHA (+223,8%)

MATERIALS   AND   METHODS

A) Study animals
The study took place in five barns of High Productive Dairy Cows (1 in VERONE and 4 in BARI – Italie lt 30/day )
– In VERONE, 20 cows were randomised in 2 groups. The treatment group receive 700g of NAT®Ω3/animal/day during 41 days. It was easy to separate the milk product from each group. However the average day of milk of the treated group was less than 30 days compared to the average day of milk from the control group
-In BARI, the 4 barns were in the same breeding methods. In each farm, 3 control and 3 treated cows were chosen at the same physiological status. The treated group received 700 of NAT®Ω3/animal/day  from 21 days before and 21 days after calving. At the end of the study only 18 cows were kept because of different events not linked to the trial.

B) Data Analisis
MILK: CSS, protein, complete fat part. Once a week
BLOOD:  Cholesterol level (HDL and LDL), Progesterone. At 21 days before calving and once a week after.
CLINICAL SIGNS: Heat control quality, BCS, Pregnant control

1. The LDL value seems to be the most important parameter
2. The LDL score increases from  21 days before calving until 7 days after calving and then decrease slowly  from 7 days until 21 days after calving
3. The HDL/LDL ratio decrease from 21 days before untll 7 days after calving
4. The HDL level does not seem to be interesting for the progesterone level and the fertility
5. The level of Progesterone in blood increase at 21 days after calving. It seems to be linked to the LDL value which increase a few days before (GUMMER 1988 – SAEZ 1983)
6. Progesterone is a profertility factor, therefore use of NAT®Ω3 (21 days before and 21 days after calving) improves the fertility results

1)  NAT®Ω3, in transition period, improve:
a) Cholesterol metabolism
b) Level of progesterone and fertility results
c) Quality of the fat part of the milk

2)  The study enables a control on dairy cows to identify the ones with a risk of low fertility results and so a prevention using NAT®Ω3