Liver phosphorus

Vig. 1. llclative activity curves of liver phosphorus fractions of rats after administration of iS ajlI PO< (103). Curve 1, total acid-soluble P 2, inorganic P 3, alcohol precipitate 4, labile P in adenosine tripliosphate 5, nonlabile P in adenosine triphos-pliate 6, Hg precipitate 7, reeidiial P 8, Pi) precipitate. The points at 105 minutes are an average of ten delermimitioris. 

Yellow phosphorus was the first identified liver toxin. It causes accumulation of lipids in the liver. Several liver toxins such as chloroform, carbon tetrachloride, and bromobenzene have since been identified. I he forms of acute liver toxicity are accumulation of lipids in the liver, hepartxiellular necrosis, iii-trahepatic cholestasis, and a disease state that resembles viral hepatitis. The types of chrome hepatotoxicity are cirrhosis and liver cancer. 

One type of fatty liver that has been smdied extensively in rats is due to a deficiency of choline, which has therefore been called a lipotropic factor. The antibiotic puromycin, ethionine (a-amino-y-mercaptobu-tyric acid), carbon tetrachloride, chloroform, phosphorus, lead, and arsenic all cause fatty liver and a marked reduction in concentration of VLDL in rats. Choline will not protect the organism against these agents but appears to aid in recovery. The action of carbon tetrachloride probably involves formation of free radicals... 

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... 

A study with a dog exposed to an occluded dermal dose of TOCP labeled with radioactive phosphorus provides limited evidence that organophosphate esters in hydraulic fluids may be widely distributed after dermal absorption (Hodge and Sterner 1943). Similar widespread distribution of radioactivity among tissues was observed in male cats after dermal exposure to [uniformly labeled 14C-phenyl]TOCP (Nomeir and Abou-Donia 1986). Tissues and fluids with the highest concentrations of radioactivity in these studies included the bile, gall bladder, urinary bladder, liver, kidney, and fat, thus suggesting that TOCP and metabolites are somewhat preferentially distributed to these tissues. 

Twenty-four hours after application of 2.094 g TOCP labeled with radioactive phosphorus to a 15x20 cm area of clipped and depilated abdominal skin, radioactivity was detected in the following tissues in a dog, listed in order of decreasing concentration (counts per gram of tissue) skin and facia at site of application, liver, omental fat, blood, kidney, lung, muscle (triceps femoris), spinal cord, heart, spleen = brain = sciatic nerve, and bone (femur) (Hodge and Sterner 1943). 

A complete physical examination and laboratory analysis are needed to rule out secondary causes and to assess kyphosis and back pain. Laboratory testing may include complete blood count, liver function tests, creatinine, urea nitrogen, calcium, phosphorus, alkaline phosphatase, albumin, thyroid-stimulating hormone, free testosterone, 25-hydroxyvitamin D, and 24-hour urine concentrations of calcium and phosphorus. Urine or serum biomarkers (e.g., cross-linked N-telopeptides of type 1 collagen, osteocalcin) are sometimes used. 

As can be seen from the results in Table V, fluoride levels in plasma, liver and kidney increased 3 to 8 times but there was no significant effect on the calcium or phosphorus content, although the kidney Ca level in fluoride treated rats was 40 higher than in the controls. Whereas the normal exposure to fluoride from air, food and water did not cause any increase in soft tissue levels, more than ten times the normal levels in soft tissues, including liver and kidney, were found in human fatalities due to fluoride poisoning (15). 

Sutherland, E.W. (1952). The effects of epinephrine and the hyperglycemic factor on liver and muscle metabolism in vitro. In Phosphorus Metabolism. (McElroy, W.D. Glass, B., Eds.), Vol. 2, pp. 577-593. The Johns Hopkins Press, Baltimore. 

Vitamin D is converted in the liver and kidneys to 1,25-dihydroxyvitamin D, which is the hormone-active compounds. The principal physiological function is to maintain the serum calcium and phosphorus concentrations in a range that support cellular processes, neuromuscular function, and bone ossihcation [417], Only a few foods contain vitamin D in quantities that have an impact on the dietary intake hsh liver, hsh liver oils, fatty fish, and egg yolks. Thus, some countries practice fortihcation of certain foods with vitamin D, most often milk, margarine, and/or butter. 

Vitamin D3 is transported to liver where it undergoes a hydroxylation at C-25 into 1a,25-dihydroxyvitamin D3 (calcitriol) (Fig. 64). In the kidney, it undergoes further hydroxylations at different sites, depending on the serum Ca + concentration. The most biologically active metabolite of vitamin D3 is calcitriol, which plays important roles in the regulation of calcium and phosphorus metabolism. It is used for treating bone diseases, but is also involved in the cell proliferation and the inducement of cell differentiation [151]. 

Holzbecher and Ellenberger have assayed chlorpromazine in liver by the use of enzyme digestion and GLC [197]. Sparagli et al. have assayed chlorpromazine after its extraction from plasma using GLC on a 3 % OV-17 or 3 % SP-2250 column [198]. In the latter method, chlorpromazine was converted to its A -trifluoroacetyl derivative prior to analysis, and a nitrogen-phosphorus detector was used in the analysis. 

An earlier cross sectional study had found that the PME/PDE ratio was a measure of disease severity in chronic hepatitis-C. ° More recently, it was found that this ratio may also serve as a biomarker of response to treatment with antiviral therapy. ° Whereas non-responders had similar or even elevated PME/PDE initially, that ratio declined from 0.27 0.02 (standard error) to 0.16 0.01 after treatment (p<0.001) in responders. Liver resection is a common therapy for liver metastases. Prior portal vein embolization (PVE) of the resected lobe results in h) ertrophy of the remaining contralateral lobe. Phosphorus-31 MRSI has been used to monitor metabolism of the regenerating lobe after PVE. ° ... 

W. C. Chu, W. W. Lam, K. H. Lee, D. K. Yeung, J. Sihoe and C.-K. Yeung, Phosphorus-31 MR spectroscopy in pediatric liver transplant recipients a noninvasive assessment of graft status with correlation with liver function tests and liver biopsy. AJR Am. J. Roentgenol, 2005,184,1624-1629. 

Phosphorus-32, for example, produced by irradiating sulphur or natural phosphorus ( P) with high-energy particles, has a half-life of 14.8 days and can be rapidly taken up (in the form of phosphate) by body tissues such as muscles, the liver, bones, and teeth. De Hevesy found that different phosphorus compounds would be incorporated in a tissue-specific manner certain compounds were concentrated in the liver, for example. One can use stable isotopes as biological tracers too, since they are detectable atom by atom using mass spectrometry. De Hevesy observed that it takes deuterium twenty-six minutes to pass from ingested heavy water into urine. 

Kirkbride (1987) described the estimation of diazinon in human omental tissue (fatty tissue) after a fatal poisoning. In this method, the tissue was pulverized and extracted with acetone. After extract concentration and purification by sweep co-distillation and Florisil fractionation, diazinon was measured by gas chromatography (GC) with nitrogen-phosphorus detection (NPD). After another fatal diazinon poisoning, diazinon was quantified by GC/electron capture detection (ECD) and GC/flame ionization detection (FID) by Poklis et al. (1980). The diazinon in human adipose, bile, blood, brain, stomach contents, kidney, and liver was recovered by macerating the sample with acetonitrile followed by the addition of aqueous sodium sulfate and extraction into hexane. Following an adsorption chromatography clean-up, the sample was analyzed. 

In 1948, red cobalt-containing crystals of vitamin B12 were obtained almost simultaneously by two pharmaceutical firms. Charcoal adsorption from liver extracts was followed by elution with alcohol and numerous other separation steps. Later fermentation broths provided a richer source. Chemical studies revealed that the new vitamin had an enormous molecular weight, that it contained one atom of phosphorus which could be released as P , a molecule of aminopropanol, and a ribofuranoside of dimethyl benzimidazole with the unusual a configuration. 

Although many phosphorus-containing compounds are vital to life processes, as previously described, there are also many phosphorus compounds that axe quite toxic—elemental phosphorus, for example. While the elemental form is dangerous because of its low combustion temperature, its absorption also has an acute effect on the liver. The long and continued absorption of small amounts of phosphorus can result in necrosis of the mandible or jaw bone (sometimes called phossyjaw ). Chronic phosphorus poisoning occurs particularly through the lungs and... 

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