Kidney , enzymes excretion products

Urea is synthesized almost exclusively in the liver and then transported to the kidneys for excretion. The process that generates urea is called the urea cycle and is depicted in Figure 20.13. Urea is synthesized almost exclusively in the liver and then transported to the kidneys for excretion. The enzyme arginase is responsible for the cyclic nature of the urea cycle and for production of urea, as follows ... 

Most of the low molecular substances that are flushed into the primary urine during ultrafiltration are reabsorbed to a large extent. This is true even for such typical excretion products as urea and uric acid, but especially for free amino acids and glucose, which are reabsorbed completely so long as the blood sugar level stays normal. If the level exceeds 0.16%, some of the sugar is excreted in the urine. Reabsorption is active transport (Chapt. XXI-3) and the enzymic apparatus of active transport can no longer cope with the amounts delivered by the blood. Similar conditions prevail for other substances the capacity for reabsorption (formerly called kidney threshold ) differs widely for various substances. 

Carbonic anhydrase is an enzyme that produces free hydrogen ions, which are then exchanged for sodium ions in the kidney tubules. Carbonic anhydrase inhibitors inhibit the action of the enzyme carbonic anhydrase This effect results in the excretion of sodium, potassium, bicarbonate, and water. Carbonic anhydrase inhibitors also decrease the production of aqueous humor in the eye, which in turn decreases intraocular pressure (IOP) (ie, the pressure within the eye). 

Copper is an essential trace element. It is required in the diet because it is the metal cofactor for a variety of enzymes (see Table 50—5). Copper accepts and donates electrons and is involved in reactions involving dismu-tation, hydroxylation, and oxygenation. However, excess copper can cause problems because it can oxidize proteins and hpids, bind to nucleic acids, and enhance the production of free radicals. It is thus important to have mechanisms that will maintain the amount of copper in the body within normal hmits. The body of the normal adult contains about 100 mg of copper, located mostly in bone, liver, kidney, and muscle. The daily intake of copper is about 2—A mg, with about 50% being absorbed in the stomach and upper small intestine and the remainder excreted in the feces. Copper is carried to the liver bound to albumin, taken up by liver cells, and part of it is excreted in the bile. Copper also leaves the liver attached to ceruloplasmin, which is synthesized in that organ. 

The answer is C. Ingestion of an acid or excess production by the body, such as in diabetic ketoacidosis, may induce metabolic acidosis, a condition in which both pH and HCOj become depressed. In response to this condition, the carbonic acid-bicarbonate system is capable of disposing of the excess acid in the form of CO2. The equilibrium between bicarbonate and carbonic acid shifts toward formation of carbonic acid, which is converted to COj and HjO in the RBC catalyzed by carbonic anhydrase, an enzyme found mainly in the RBC. The excess CO2 is then expired by the lungs as a result of respiratory compensation for the acidosis (Figure 1-2). The main role of the kidneys in managing acidosis is through excretion of H" rather than CO2. 

Most glucocorticosteroid are metabolized in the liver to hydroxy- and ketosteroid metabolites which are excreted by the kidneys as glucuronides, sulfates and unconjugated products. Enzyme-inducing agents will diminish the efficacy of glucocorticosteroids. 

The metabolic study, considered separately, consists of treatment of the animal with the radiolabeled compound followed by chemical analysis of all metabolites formed in vivo and excreted via the lungs, kidneys, or bile. Although reactive intermediates are unlikely to be isolated, the chemical structure of the end products may provide vital clues to the nature of the intermediates involved in their formation. The use of tissue homogenates, subcellular fractions, and purified enzymes may serve to clarify events occurring during metabolic sequences leading to the end products. 

Induction of extrahepatic mdoleamine dioxygenase (which catalyzes the same reaction as tryptophan dioxygenase, albeit by a different mechanism) by bacterial lipopolysaccharides and mterferon-y may result in the production of relatively large amounts of kynurenine and hydroxykynurenine in tissues that lack the enzymes for onward metabolism. Kidney has kynurenine transaminase activity, and therefore extrahepatic metabolism of tryptophan may result in significant excretion of kynurenic and xanthurenic acids, even when vitamin Bg nutrition is adequate. 

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