Gil, Enrique. Protein Metabolism in Ruminants. Library. College of Agricultural Sciences (UNMP). Balcarce. Argentina. 1994.

Summary
The rumen is of primary importance when considering protein nutrition, and the concepts of protein digestion in the non ruminant animals cannot be applied to the ruminant.
It would seem that the simplest and most profitable way for rumen micro-organisms to digest food proteins would be to assimilate them directly into microbial protein using the high energy phosphate available from fermentation. The aminoacids of the food would become the aminoacids of the microbes. Although this may occur in some anaerobic bacteria, the major metabolic process in the rumen is the fermentation of the protein to provide energy and ammonia. The ammonia may in turn be assimilated again by the bacteria and transformed into protoplasmic protein. Ammonia cannot be assimilated by the ruminal bacteria unless a carbohydrate source is available. The relative importance of proteins as energy or as monomers for bacterial cell synthesis depends on the ratio of carbohydrate to nitrogen in the rumen. The problem of following the digestion of feed protein in the rumen is complicated by the fact that, as feed protein is digested, microbial protein is synthesised, and the rates of the two processes are not easy to measure separately. Nevertheless, bacterial protein can be distinguished from plant protein and protozoa protein by measuring the amount of 2,6 diaminopimelic acid. This component of the cell wall of most bacteria and blue-green algae does not occur in animals and higher plants. There is no doubt that rumen bacteria certainly posses an active proteolitic activity. The bacteria appear to synthesise all their cell nitrogen from ammonium salts and use glucose as a source of energy. The enzyme is mostly intracellular, associated with the cell wall fraction. The importance to the animal of the proteolytic activity within the rumen is that it liberates aminoacids which may then be deaminated. If the degradation stopped at the hydrolysis level, the nutrition of the animal would be very little affected, as protein hydrolysis would subsequently have occurred in the abomasum and duodenum. Since hydrolysis must precede deamination, attempts have been made to reduce deamination in the rumen by reducing proteolysis. The most common method has been to reduce the solubility of the feed protein. Nevertheless, should microbial protein synthesis be impaired, great care must be considered as to the protein quality consumed by the animal, as the Biological Value of microbial protein is usually superior to natural forage protein. One of the most intriguing problems in rumen ecology is the extent to which ammonia serves as the nitrogenous material for synthesis of microbial cell protoplasm. There are limits as to the amounts of nitrogenous substrate which a ruminant micro-organism can assimilate. Aminoacids in excess of that limit will be available for supplying energy, and ammonia will appear to the extent that the available aminoacids exceed their assimilation into microbial cells.
The Path to alfa-Amino Groups. There is an array of mechanisms by which ammonia may be liberated from preformed æ-amino groups. Only two of these, however are reversible,and these two reactions (aspartic deaminase, or aspartase; glutamic deaminase, or glutamic dehydrogenase), constitute the only pathways known by which ammonia may be converted into alfa-amino groups. This fact is indeed surprising, for one would certainly expect a variety of pathways by which an essential material such as nitrogen is assimilated by the microbial cells. The fumarate gateway is dependent upon the reaction between an unsaturated dicarboxy acid, fumaric acid and ammonia to yield aspartic acid. The aspartic acid once formed can be transaminated with alfa-ketoglutarate (plus oxaloacetate which may be reduced to malate, which may be dehydrated to fumarate ready to pick up another ammonia molecule). This pathway requires the backup of the carbohydrate metabolism and is the major pathway used by the ruminal bacteria when they use the ammonia nitrogen produced by non protein nitrogen sources such as urea. Mainly oxaloacetic (pyruvic acid plus CO₂) is the only source it has of obtaining the necessary keto groups (C=O), required for the synthesis of aminoacids. The ketoglutarate gateway is dependent upon a reaction involving an alfa-ketodicarboxy acid and thus involves a hydrogenation, and the product produced is L-glutamic acid. The enzyme is linked to either DPN or TPN. In some cases to both, depending on the rumen micro-organisms involved. Very possibly this gateway is the major path by which aminoacids are synthesised from ammonia obtained by aminoacid deamination as this process produces at the same time the ketoacid (C=O) required, from the deaminated aminoacid.
Urea Toxicity. It has been known now for many years that rumen micro-organisms are capable of utilising nitrogen sources from non protein nitrogen (NPN) compounds such as urea. However the feeding of urea or other NPN compounds may result in toxicity and death when overfed or under determined conditions such as combining in the ration true protein nitrogen and NPN combinations. Toxicity symptoms from over consumption of NPN develop rapidly (within 30 to 60 minutes) after ingestion of the toxic dose. This is a reflection, no doubt, of the high urease activity of the rumen liquor. The general opinion in that the ammonium ion is the toxic factor, due to the fact that a noticeable increase in blood ammonia is noted in conjunction with toxicity of urea and other NPN compounds. Death that can occur within two hours is usually thought to be due to alkalosis caused by the rapid liberation of ammonia. Nevertheless, in spite of the rumen and blood dysfunction due to this alkalosis situation there is a nervous factor observed due to the ammonia per se, as the responsible factor for this syndrome. I suggest that the following metabolic steps are taking place: a). a substance known as ammonium carbamate has been found in the rumen liquor and blood of urea intoxicated animals. The ammonium carbamate formed by the hydrolysis of urea is converted in part into formic acid, which in the presence of nitrate and molybdenum may further be oxidised to: oxalic acid. b). The nervous syndrome can be due to the fact that oxalic acid structurally competes for the "locus" that is occupied by calcium that metabolically activates succinate dehydrogenase in the succinate <=> fumarase pathway in the citric acid cycle, and in so doing impairs the energy requirements of the nervous system. It is also possible that the oxalic acid combines with the blood calcium forming calcium oxalate, situation that would also deplete the required calcium within the system.

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