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Liver minerals

Chicken, liver -mineral nutrient source [MINERAL NUTRIENTS] (Vol 16)... [Pg.192]

Arsenic Skin, lung, liver Miners and smelters, oil refinery, pesticide workers... [Pg.46]

A low germanium intake has been found to alter bone and liver mineral composition and decrease tibial DNA in rats. Germanium also reverses changes in rats caused by silicon deprivation, and is touted as having anticancer properties because some organic complexes of germanium can inhibit tumor formation in animal models. [Pg.406]

Carcinogens Cancer-producing agents Skin Respiratory Bladder/urinary tract Liver Nasal Bone marrow Coal tar pitch dust crude anthracene dust mineral oil mist arsenic. Asbestos polycyclic aromatic hydrocarbons nickel ore arsenic bis-(chloromethyl) ether mustard gas. p-naphthylamine benzidine 4-am i nodi pheny lam ine. Vinyl chloride monomer. Mustard gas nickel ore. Benzene. [Pg.69]

Nitrogen sources include proteins, such as casein, zein, lactalbumin protein hydrolyzates such proteoses, peptones, peptides, and commercially available materials, such as N-Z Amine which is understood to be a casein hydrolyzate also corn steep liquor, soybean meal, gluten, cottonseed meal, fish meal, meat extracts, stick liquor, liver cake, yeast extracts and distillers solubles amino acids, urea, ammonium and nitrate salts. Such inorganic elements as sodium, potassium, calcium and magnesium and chlorides, sulfates, phosphates and combinations of these anions and cations in the form of mineral salts may be advantageously used in the fermentation. [Pg.1062]

Acid- and alkaline phosphatases act on a variety of mono- and multiple phosphate carrying low molecular mass molecules. In addition, they hydrolyze many, but not all, phosphoproteins. They are in use for decades to easily screen for diseases, however, somewhat unspe-cifially. For instance, acid phosphatase is used as biomarker for prostate cancer, and alkaline phosphatase to monitor bone (de-) mineralization and liver tumors. [Pg.1015]

In bone, three proteins have been described which are vitamin K-dependent, osteocalcin (bone Gla protein), matrix Gla protein (MGP), and protein S. Osteocalcin is synthetized by osteoclasts, regulated by the active form of vitamin D, calcitriol. Its capacity to bind calcium needs a vitamin K-dependent y-carboxylation of three glutamic acid residues. The calcium binding capacity of osteocalcin indicates a possible role in bone mineralization, but its exact function is still unclear. However, it is widely used as a serum marker for bone mineralization. Protein S, mainly a coagulant, is also vitamin-K dependent and synthesized in the liver. Children with... [Pg.1299]

The above scientific information on rice bran phytochemicals indicates that a multitude of mechanisms are operating at the cellular level to bring about specific health effects. Several health benefits of rice bran appear to be the result of the synergistic function of the many phytochemicals, antioxidants, vitamins and minerals which operates through a specific immune response. Their role in the biochemical mechanisms at the cellular level which result in major health effects is shown in Fig. 17.1. A short overview summarizing the effect of the various phytochemicals on major health issues such as cancer, immune function, cardiovascular disease, diabetes, altered liver function and gastrointestinal and colon disease will be given below. [Pg.363]

The sinusoids transport both portal and arterial blood to the hepatocytes. The systemic blood delivered to the liver contains nutrients, drugs, and ingested toxins. The liver processes the nutrients (carbohydrates, proteins, lipids, vitamins, and minerals) for either immediate use or for storage, while the drugs and toxins are metabolized through a variety of processes known as first-pass metabolism. The liver also processes metabolic waste products for excretion. In cirrhosis, bilirubin (from the enzymatic breakdown of heme) can accumulate this causes jaundice (yellowing of the skin), scleral icterus (yellowing of the sclera), and tea-colored urine (urinary bilirubin excretion). [Pg.325]

Mineral oil may accumulate to some degree in liver and fatty tissues after absorption of ingested mineral oil hydraulic fluids, as indicated by experiments with rats given single, 0.66-mL, oral doses of tritiated mineral oil (Ebert et al. 1966). Twenty-four hours after administration, the concentrations of tritiated mineral oil in liver and fat were approximately seven-fold greater than those in kidney and brain other tissues were not examined. [Pg.168]

Based on physical and chemical similarities between mineral oil and polyalphaolefins, oil accumulation in the lung (and subsequent lipoid pneumonia) may occur following the ingestion of polyalphaolefin hydraulic fluids due to aspiration, and that distribution of polyalphaolefins to the liver and fatty tissues may occur to some degree (see discussion for distribution of mineral oil hydraulic fluids). [Pg.170]

Experiments with monkeys given intramuscular injections of a mineral oil emulsion with [l-14C] -hexa-decane tracer provide data illustrating that absorbed C-16 hydrocarbon (a major component of liquid petrolatum) is slowly metabolized to various classes of lipids (Bollinger 1970). Two days after injection, substantial portions of the radioactivity recovered in liver (30%), fat (42%), kidney (74%), spleen (81%), and ovary (90%) were unmetabolized -hexadecane. The remainder of the radioactivity was found as phospholipids, free fatty acids, triglycerides, and sterol esters. Essentially no radioactivity was found in the water-soluble or residue fractions. One or three months after injection, radioactivity still was detected only in the fat-soluble fractions of the various organs, but 80-98% of the detected radioactivity was found in non-hydrocarbon lipids. [Pg.171]

Mineral Oil Hydraulic Fluids. No studies regarding hepatic effects in humans following inhalation, oral, or dermal exposure to mineral oil hydraulic fluids were located. In an animal study, histopathological examination of the livers from rats exposed by inhalation to <1.0 mg/m3 of the water-in-oil emulsion hydraulic fluid Houghto-Safe 5047F for 90 days, 23 hours/day, showed no treatment-related lesions (Kinkead et al. 1991). Animal data for oral exposure are limited to one study where rats were exposed to MIL-H-5606 at 1,000 mg/kg/day for 26 days (Mattie et al. 1993). Increases in liver weight and peroxisomal beta-oxidation activity were observed. [Pg.201]

Absorbed hydrocarbons from mineral oil are likely to be preferentially distributed to the liver and fatty tissues and slowly metabolized to various types of lipids. Polyalphaolefins are expected to be similarly distributed and retained based on the similarities of the physical and chemical properties of polyalphaolefins and mineral oil. [Pg.232]

Vermilion and cinnabar are two bright red, toxic minerals that share an identical composition (they are both composed of mercury sulfide) but have different crystal structures. Two kinds of vermilion are known one of natural origin and another made artificially. Finely ground natural vermilion may vary in hue from red to liver-brown and even to black. Artificial vermilion was made from mercury and sulfur the method of preparation seems to have been developed by the Chinese and was introduced into Europe only during the eighth century c.e. (Gettens et al. 1972). [Pg.97]

Cytotoxicity of methylamine [45], kidney liver and myocardial damage due to ethylamine [46], hepatosplenomegaly and eosinophilia due to aniline [47], euphoria, dyspnea, teratogenicity, renal failure, hematuria, proteinurea, anorexia and methanoglobinemia due to a-naphthylamine and diphenylamine have been reported in the literature [48-54]. Therefore the remediation and mineralization of amines is... [Pg.316]

Kume, S., A. Mukai, and M. Shibata. 1984. Effects of dietary copper and molybdenum levels on liver and kidney minerals in Holstein cattle. Japan. Jour. Zootech. Sci. 55 670-676. [Pg.1575]

One case study was identified where a man who had been occupationally exposed to hexachloroethane was treated for a liver tumor (Selden et al. 1989). Exposure had occurred over a period of 6 years as a result of the presence of hexachloroethane in a degassing agent used during aluminum smelting. However, the hexachloroethane reacted at the 700 C use-temperature, releasing a gas that was 96% hexachlorobenzene with small amounts of other chlorinated compounds. Because there was occupational exposure to a mixture of chlorinated compounds rather than just hexachloroethane, it is highly unlikely that the tumor was the result of hexachloroethane exposure alone. Occupational exposure to mineral oil mists for 20 years was also part of the subject s employment history. [Pg.44]

On the other hand, in rats, a single dose of 6,156 mg/kg hexachloroethane in mineral oil had no effects on a different set of biochemical indicators of liver function (microsomal protein, oxidative demethylase, NADP-NT reductase, glucose-6-phosphatase, or lipid conjugated diene concentration) when measured 2 hours after compound administration (Reynolds 1972). Each of these parameters is an indicator of microsomal function. The authors postulated that the observed lack of effects could have been the result of slow uptake of hexachloroethane by the liver in a 2-hour period. Gastrointestinal absorption of hexachloroethane in mineral oil is probably minimal because, unlike olive oil, mineral oil cannot be digested. Dissolved lipophilic materials could be excreted in the feces soon after administration because mineral oil can act as a laxative. Thus, the author s hypothesis that minimal hexachloroethane would reach the liver in 2 hours is reasonable. [Pg.59]

Animal data suggest that renal and liver effects may occur in humans exposed to high doses of hexachloroethane. Kidney and liver effects are not specific to hexachloroethane. Lesions of the kidney (nephropathy, linear mineralization, and hyperplasia) were reported at 10 mg/kg/day or greater in male rats (NTP 1989). Urinalysis also revealed granular and cellular casts in rats exposed to hexachloroethane (47 mg/kg/day or greater) for 13 weeks (NTP 1989). Because other compounds cause similar effects and because some of these effects are unique to male rats, they are not valuable as biomarkers for human hexachloroethane exposure. [Pg.97]

Extremely stringent lower limits were reported by Rank (29) in 1968. A spectroscopic detection of the Lyman a(2 p - 1 s) emission line of the quarkonium atom (u-quark plus electron) at 2733 A was expected to be able to show less than 3 108 positive quarks, to be compared with 1010 lithium atoms detected by 2 p - 2 s emission at 6708 A. With certain assumptions (the reader is referred to the original article), less than one quark was found per 1018 nucleons in sea water and 1017 nucleons in seaweed, plankton and oysters. Classical oil-drop experiments (with four kinds of oil light mineral, soya-bean, peanut and cod-liver) were interpreted as less than one quark per 1020 nucleons. Whereas a recent value (18) for deep ocean sediments was below 10 21 per nucleon, much more severe limits were reported (30) in 1966 for sea water (quark/nucleon ratio below 3 10-29) and air (below 5 10-27) with certain assumptions about concentration before entrance in the mass spectrometer. At the same time, the ratio was shown to be below 10 17 for a meteorite. Cook etal. (31) attempted to concentrate quarks by ion-exchange columns in aqueous solution, assuming a position of elution between Na+ and Li+. As discussed in the next section, cations with charge + 2/3 may be more similar to Cs+. Anyhow, values below 10 23 for the quark to nucleon ratio were found for several rocks (e.g., volcanic lava) and minerals. It is clear that if such values below a quark per gramme are accurate, we have a very hard time to find the object but it needs a considerably sophisticated technique to be certain that available quarks are not lost before detection. [Pg.31]

Phosphates of pharmaceutical interest are often monoesters (Sect. 9.3), and the enzymes that are able to hydrolyze them include alkaline and acid phosphatases. Alkaline phosphatase (alkaline phosphomonoesterase, EC 3.1.3.1) is a nonspecific esterase of phosphoric monoesters with an optimal pH for catalysis of ca. 8 [140], In the presence of a phosphate acceptor such as 2-aminoethanol, the enzyme also catalyzes a transphosphorylation reaction involving transfer of the phosphoryl group to the alcohol. Alkaline phosphatase is bound extracellularly to membranes and is widely distributed, in particular in the pancreas, liver, bile, placenta, and osteoplasts. Its specific functions in mammals remain poorly understood, but it seems to play an important role in modulation by osteoplasts of bone mineralization. [Pg.56]


See other pages where Liver minerals is mentioned: [Pg.537]    [Pg.490]    [Pg.537]    [Pg.490]    [Pg.92]    [Pg.139]    [Pg.156]    [Pg.88]    [Pg.318]    [Pg.61]    [Pg.42]    [Pg.160]    [Pg.162]    [Pg.167]    [Pg.241]    [Pg.432]    [Pg.283]    [Pg.710]    [Pg.200]    [Pg.539]    [Pg.1551]    [Pg.1608]    [Pg.274]    [Pg.333]    [Pg.81]    [Pg.120]    [Pg.212]    [Pg.61]    [Pg.342]    [Pg.254]   
See also in sourсe #XX -- [ Pg.59 ]




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