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Lead, liver content

Niacin (vitamin B3) has broad applications in the treatment of lipid disorders when used at higher doses than those used as a nutritional supplement. Niacin inhibits fatty acid release from adipose tissue and inhibits fatty acid and triglyceride production in liver cells. This results in an increased intracellular degradation of apolipoprotein B, and in turn, a reduction in the number of VLDL particles secreted (Fig. 9-4). The lower VLDL levels and the lower triglyceride content in these particles leads to an overall reduction in LDL cholesterol as well as a decrease in the number of small, dense LDL particles. Niacin also reduces the uptake of HDL-apolipoprotein A1 particles and increases uptake of cholesterol esters by the liver, thus improving the efficiency of reverse cholesterol transport between HDL particles and vascular tissue (Fig. 9-4). Niacin is indicated for patients with elevated triglycerides, low HDL cholesterol, and elevated LDL cholesterol.3... [Pg.189]

Evidence suggests that lead exacerbates the toxic effects of mercury. In the rat, the administration of lead nitrate increased kidney and liver glutathione content and resulted in increased mercury deposition in the kidney, along with increased lethality in rats (Congiu et al. 1979). [Pg.329]

Tissue lead (mg/kg FW) 0.81 in blood, 26.4 in liver, 50.3 in kidney, and 400 in rumen contents Calves given 2.7 mg Pb/kg body weight (BW), as lead acetate, for 20 days milk diet Calves given 3.0 to 3.5 mg Pb/kg BW daily for 3 months grain and hay diet Calves given 5 mg Pb/kg BW, as Pb acetate, for 7 days grain and hay diet Calves given 5 mg Pb/kg BW, as Pb acetate, for 7 days milk diet... [Pg.310]

B excess Aral-Caspian low plain, Kazakhstan Brunozems, Solonetses, and Solonchaks are enriched in B, up to 280 ppm. The increased content of B in forage species, up to 0.15% by dry weight Accumulation of B in animal organisms leads to the disturbance of B excretion function of liver, reducing activity of amilase and, partly, of proteinase of the intestine tract in human and sheep. Endemic boron ententes sometimes accomplished by pneumonia. Human, sheep and camel morbidity... [Pg.42]

Ethanol-related high levels of NADH+H and acetyl-CoA in the liver lead to increased synthesis of neutral fats and cholesterol. However, since the export of these in the form of VLDLs (see p. 278) is reduced due to alcohol, storage of lipids occurs (fatty liver). This increase in the fat content of the liver (from less than 5% to more than 50% of the dry weight) is initially reversible. However, in chronic alcoholism the hepatocytes are increasingly replaced by connective tissue. When liver cirrhosis occurs, the damage to the liver finally reaches an irreversible stage, characterized by progressive loss of liver functions. [Pg.320]


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