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Albumin metabolism

Chromium has proved effective in counteracting the deleterious effects of cadmium in rats and of vanadium in chickens. High mortality rates and testicular atrophy occurred in rats subjected to an intraperitoneal injection of cadmium salts however, pretreatment with chromium ameliorated these effects (Stacey et al. 1983). The Cr-Cd relationship is not simple. In some cases, cadmium is known to suppress adverse effects induced in Chinese hamster (Cricetus spp.) ovary cells by Cr (Shimada et al. 1998). In southwestern Sweden, there was an 80% decline in chromium burdens in liver of the moose (Alces alces) between 1982 and 1992 from 0.21 to 0.07 mg Cr/kg FW (Frank et al. 1994). During this same period in this locale, moose experienced an unknown disease caused by a secondary copper deficiency due to elevated molybdenum levels as well as chromium deficiency and trace element imbalance (Frank et al. 1994). In chickens (Gallus sp.), 10 mg/kg of dietary chromium counteracted adverse effects on albumin metabolism and egg shell quality induced by 10 mg/kg of vanadium salts (Jensen and Maurice 1980). Additional research on the beneficial aspects of chromium in living resources appears warranted, especially where the organism is subjected to complex mixtures containing chromium and other potentially toxic heavy metals. [Pg.95]

Pharmacokinetics Rapidly absorbed from the Glfracf. Protein binding 18%. Distributed to blood cells binds to plasma proteins, mainly albumin. Metabolized in the liver. Excreted in urine. Half-life 7 hr. [Pg.550]

Pharmacokinetics Well absorbed after PO administration. Binds to plasma proteins, particularly albumin. Metabolized in the liver. Eliminated mainly in the feces as metabolites. Half-life 18 hr. [Pg.613]

Pharmacokinetics Moderately absorbed from the gastrointestinal (GI) tract. Protein binding 80% to albumin. Metabolized in small amounts in liver. Excreted unchanged... [Pg.950]

Pharmacokinetics Absorption differs between formulations. Protein binding 50%-80%. Bound to serum albumin. Metabolized to salicylate glucuronides and salicyluric acid. Excreted in urine. [Pg.1108]

Mecfianism of Action An NSAID that inhibits prostaglandin synthesis, reducing the inflammatory response and the intensity of pain stimuli reaching the sensory nerve endings. Therapeutic Effect Produces analgesic and anti-inflammatory effects. Pharmacokinetics Rapidly and completely absorbed from the G1 tract. Food delays absorption of salsalate. Protein binding Fligh (to albumin). Metabolized in the liver. Excreted in urine. Removed by hemodialysis. Half-life 1 hr. [Pg.1111]

Example Isotretinoin (Accutane) Route PO Pregnancy category X Pharmacokinetic Absorption enhanced when taken with a high-fat meal. It binds to plasma proteins (albumin), metabolized in the liver and excreted in feces and urine. [Pg.318]

In many acute conditions, priority on the part of the blood volume regulation as compared to regulation of albumin metabolism must account... [Pg.256]

Estrogen RBA to SHBG % Bound to SHBG % Bound to Albumin Metabolic Clearance Rate (litter/day/m )... [Pg.2068]

EoUowing po administration moricizine is completely absorbed from the GI tract. The dmg undergoes considerable first-pass hepatic metabolism so that only 30—40% of the dose is bioavailable. Moricizine is extensively (95%) bound to plasma protein, mainly albumin and a -acid glycoprotein. The time to peak plasma concentrations is 0.42—3.90 h. Therapeutic concentrations are 0.06—3.00 ]l/niL. Using radiolabeled moricizine, more than 30 metabolites have been noted but only 12 have been identified. Eight appear in urine. The sulfoxide metabolite is equipotent to the parent compound as an antiarrhythmic. Elimination half-life is 2—6 h for the unchanged dmg and known metabolites, and 84 h for total radioactivity of the labeled dmg (1,2). [Pg.113]

The absorption of metoprolol after po dosing is rapid and complete. The dmg undergoes extensive first-pass metabolism in the liver and only 50% of the po dose in bioavailable. About 12% of the plasma concentration is bound to albumin. The elimination half-life is 3—7 h and less than 5% of the po dose is excreted unchanged in the urine. The excretion of the dmg does not appear to be altered in patients having renal disease (98,99,108). [Pg.127]

Data from a single study in dogs suggest that hepatic first-pass metabolism may limit systemic availability of the parent compound following oral exposure (Braeckman et al. 1983). Placental transfer of methyl parathion was demonstrated in pregnant rats 1-3 days before parturition. Thirty minutes after administration, both methyl parathion and methyl paraoxon were found in fetal brain, liver, and muscle methyl parathion, but not methyl paraoxon, was detected in placenta and maternal liver (Ackermann and Engst 1970). Methyl parathion binds reversibly to serum albumin, but is readily distributed to the tissues (Braeckman et al. 1980, 1983). [Pg.100]

Bilirubin formed in peripheral tissues is transported to the hver by plasma albumin. The further metabolism of bihtubin occuts primarily in the hver. It can be divided into thtee processes (1) uptake of bilirubin by hver parenchymal cells, (2) conjugation of bilirubin with glucuronate in the endoplasmic reticulum, and (3) secretion of conjugated bilirubin into the bile. Each of these processes will be considered separately. [Pg.280]

In the liver, the bilirubin is removed from albumin and taken up at the sinusoidal surface of the hepato-cytes by a carrier-mediated saturable system. This facilitated transport system has a very large capacity, so that even under pathologic conditions the system does not appear to be rate-limiting in the metabolism of bilirubin. [Pg.280]

This scheme shows that cyanide sourced from smoking or otherwise (see 6.3.7) may determine the metabolism of chrysotherapeutic agents. [Au(CN)2] anions bind to serum albumin predominantly by the formation of adducts without the displacement of cyanide [94]. The ions bind tightly to albumin independent of the oxidative state of Cys-34. The equilibrium constant values for [Au(CN)2] binding to serum albumin are similar to values for other gold complexes that bind to albumin. This indicates that albumin can act as a carrier for transporting [Au(CN)2] in the bloodstream. [Pg.297]

Isab, A.A., Shaw, C.E. Ill and Locke, J. (1988) GC-MS and oxygen-17 NMR tracer studies of triethylphosphine oxide formation from auranofin and water- O in the presence of bovine serum albumin an in vitro model for auranofin metabolism. Inorganic Chemistry, 27, 3406-3409. [Pg.315]

Decreased red blood cell (RBC) count, hemoglobin (Hgb) and hematocrit (Hct) iron metabolism may also be altered [iron level, total iron binding capacity (TIBC), serum ferritin level, and transferrin saturation (TSAT)]. Erythropoietin levels are not routinely monitored and are generally normal to low. Urine positive for albumin or protein. [Pg.378]

Approximately 80% of patients with a GFR less than 20 to 30 mL/minute develop metabolic acidosis.38 Metabolic acidosis can increase protein catabolism and decrease albumin synthesis, which promote muscle wasting, and alter bone metabolism. Other consequences associated with metabolic acidosis in CKD include worsening cardiac disease, impaired glucose tolerance, altered growth hormone and thyroid function, and inflammation.38... [Pg.392]

Any time an ABG is analyzed it is wise to concurrently inspect the serum chemistry values to calculate the anion gap. The body does not generate an anion gap to compensate for a primary disorder. As such, if the calculated anion gap exceeds 12 mEq/L (mmol/L) there is a primary metabolic acidosis regardless of the pH or the serum HC03 concentration. The anion gap may be artificially lowered by decreased serum albumin, multiple myeloma, lithium intoxication, or a profound increase in the serum potassium, calcium, or magnesium. [Pg.424]

Liver function, including AST, ALT, alkaline phosphatase, lactate dehydrogenase (LDH), total and conjugated bilirubin a comprehensive metabolic panel can be ordered (i.e., sodium, potassium, chloride, bicarbonate, blood urea nitrogen, creatinine, glucose, calcium, AST, ALT, alkaline phosphatase, albumin, and total bilirubin), but phosphorus, magnesium, and fractionated... [Pg.1508]

AC ADME ANS AUC BA/BE BBB BBM BBLM BCS BLM BSA CE CHO CMC CPC CPZ CTAB CV DA DOPC DPPC DPPH aminocoumarin absorption, distribution, metabolism, excretion anilinonaphthalenesulfonic acid area under the curve bioavailability-bioequivalence blood-brain barrier brush-border membrane brush-border lipid membrane biopharmaceutics classification system black lipid membrane bovine serum albumin capillary electrophoresis caroboxaldehyde critical micelle concentration centrifugal partition chromatography chlorpromazine cetyltrimethylammonium bromide cyclic votammetry dodecylcarboxylic acid dioleylphosphatidylcholine dipalmitoylphosphatidylcholine diphenylpicrylhydrazyl... [Pg.304]


See other pages where Albumin metabolism is mentioned: [Pg.210]    [Pg.77]    [Pg.142]    [Pg.332]    [Pg.210]    [Pg.77]    [Pg.142]    [Pg.332]    [Pg.224]    [Pg.224]    [Pg.224]    [Pg.273]    [Pg.468]    [Pg.165]    [Pg.124]    [Pg.494]    [Pg.303]    [Pg.205]    [Pg.283]    [Pg.587]    [Pg.224]    [Pg.225]    [Pg.197]    [Pg.176]    [Pg.361]    [Pg.685]    [Pg.150]    [Pg.406]    [Pg.1524]    [Pg.257]    [Pg.679]    [Pg.226]   
See also in sourсe #XX -- [ Pg.151 ]




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Protein metabolism - albumin

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