Hepatic cells

Liver and Gallbladder. High dosages of oral estrogens have been reported to increase the risk for jaundice, cholestatic hepatitis, gallstones, and hepatic vein blood clots. Estrogens promote the development of hepatic neoplasms associated with increased hepatic cell regenerative activity (186,187). [Pg.245]

Historical Inhalation Agents. Diethyl ether produces excellent surgical anesthesia, but it is flammable (see Ethers). Chloroform is a nonflammable, sweet smelling, colorless Hquid which provides analgesia at nonanesthetic doses and can provide potent anesthesia at 1% (see Chlorocarbons AND CHLOROHYDROCARBONs). However, a metabohte causes hepatic cell necrosis. Tdlene, a nonflammable colorless Hquid, has a slower onset and recovery and a higher toxicity and chemical reactivity than desirable. Cyclopropane is a colorless gas which has rapid induction (2 —3 min) and recovery characteristics and analgesia is obtained in the range of 3—5% with adequate skeletal muscle relaxation (see Hydrocarbons). The use of cyclopropane has ceased, however, because of its flammabiHty and marked predisposition to cause arrhythmias. [Pg.408]

In-vitro models can provide preliminary insights into some pharmacodynamic aspects. For example, cultured Caco 2 cell lines (derived from a human colorectal carcinoma) may be used to simulate intestinal absorption behaviour, while cultured hepatic cell lines are available for metabolic studies. However, a comprehensive understanding of the pharmacokinetic effects vfill require the use of in-vivo animal studies, where the drug levels in various tissues can be measured after different dosages and time intervals. Radioactively labelled drugs (carbon-14) may be used to facilitate detection. Animal model studies of human biopharmaceutical products may be compromised by immune responses that would not be expected when actually treating human subjects. [Pg.64]

Dubois M, Plaisance H, Thome JP, et al. 1996. Hierarchical cluster analysis of environmental pollutants through P450 induction in cultured hepatic cells. Ecotoxicol Environ Saf 34 205-215. [Pg.202]

The chronic-duration oral MRL was derived based on the observation of increased serum levels of alkaline phosphatase (an indicator of hepatotoxicity) in dogs consuming 0.6 mg/kg/day for 1 year (Hoechst 1989c). The choice of this end point is supported by the observation of hydropic hepatic cells in rats that consumed 5 mg/kg/day for 2 years (EMC 1959b). The chronic-duration MRL of 0.002 mg/kg/day was derived by dividing the NOAEL for elevated serum alkaline phosphatase (0.18 mg/kg/day) by an uncertainty factor of 100 (10 for extrapolating from animals to humans, and 10 for human variability). [Pg.147]

Swagell CD, Henly DC, Morris CP. Expression analysis of a human hepatic cell line in response to palmitate. Biochem Biophys Res Commun 2005 328 432-41. [Pg.165]

The citric acid cycle is the final common pathway for the aerobic oxidation of carbohydrate, lipid, and protein because glucose, fatty acids, and most amino acids are metabolized to acetyl-CoA or intermediates of the cycle. It also has a central role in gluconeogenesis, lipogenesis, and interconversion of amino acids. Many of these processes occur in most tissues, but the hver is the only tissue in which all occur to a significant extent. The repercussions are therefore profound when, for example, large numbers of hepatic cells are damaged as in acute hepatitis or replaced by connective tissue (as in cirrhosis). Very few, if any, genetic abnormalities of citric acid cycle enzymes have been reported such ab-normahties would be incompatible with life or normal development. [Pg.130]

Figure 25-2. The formation and secretion of (A) chylomicrons by an intestinal cell and (B) very low density lipoproteins by a hepatic cell. (RER, rough endoplasmic reticulum SER, smooth endoplasmic reticulum G, Golgi apparatus N, nucleus C, chylomicrons VLDL, very low density lipoproteins E, endothelium SD, space of Disse, containing blood plasma.) Apolipoprotein B, synthesized in the RER, is incorporated into lipoproteins in the SER, the main site of synthesis of triacylglycerol. After addition of carbohydrate residues in G, they are released from the cell by reverse pinocytosis. Chylomicrons pass into the lymphatic system. VLDL are secreted into the space of Disse and then into the hepatic sinusoids through fenestrae in the endothelial lining.

This reaction helps transfer certain amino acids across the plasma membrane, the amino acid being subse-quendy hydrolyzed from its complex with GSH and the GSH being resynthesized from cysteinylglycine. The enzyme catalyzing the above reaction is 7-glu-tamyltransferase (GGT). It is present in the plasma membrane of renal mbular cells and bile ducmle cells, and in the endoplasmic reticulum of hepatocytes. The enzyme has diagnostic value because it is released into the blood from hepatic cells in various hepatobihary diseases. [Pg.630]

Walle, T. Vincent, T. S. Walle, U. K. Evidence of covalent binding of the dietary flavonoid quercetin to DNA and protein in human intestinal and hepatic cells. Biochem. Pharmacol. 2003, 65, 1603-1610. [Pg.356]

Cirrhosis is the progressive replacement of normal hepatic cells by fibrous scar tissue. This scarring is accompanied by the loss of viable hepatocytes, which are the functional cells of the liver. Progressive cirrhosis is irreversible and leads to portal hypertension that is in turn responsible for many of the complications of advanced liver disease. These consequences include (but are not limited to) spontaneous bacterial peritonitis (SBP), hepatic encephalopathy, and variceal bleeding.1... [Pg.323]

Antibodies against HCV (anti-HCV) in the blood indicate infection with the HCV. If the infection persists for more than 6 months and viral replication is confirmed by HCV RNA levels, then the person has chronic hepatitis C. Chronic disease may be due to an ineffective host immune system against the HCV. Cytotoxic T lymphocytes are ineffective in eradicating the HCV, thus allowing persistent damage to hepatic cells. Therefore, immunocompromised individuals are less likely to eliminate HCV.12... [Pg.347]

Diagnosing viral hepatitis may be difficult because most infected individuals are asymptomatic. Because symptoms cannot identify the specific type of hepatitis, laboratory serologies must be obtained (Table 21-2). In addition, liver function tests may be obtained to assess the extent of cholestatic and hepatocellular injury. However, the definitive test to determine the amount of damage and inflammation of hepatic cells is a liver biopsy. [Pg.348]

Fatty infiltration of the liver. In this pathology, the triglyceride concentration in the liver is 10-fold superior to the norm. The accumulation of fat in the cyto-plasm of hepatic cells leads to an impaired liver function. The causes of this pathol-ogy are numerous one of these may be a deficiency in lipotropic factors and the associated therewith synthesis of excess triglycerides. [Pg.213]

When high-specific-activity, non-colloidal preparations are administered (a) they are partitioned characteristically between liver and bone (b) in rodents the rate of loss of the liver burden is high (halftime = 6.5 to 10.8 d) (Durbin, 1973) (c) the spleen content is low and (d) autoradiographs show uniform distribution in hepatic cells rather than of phagocytosis of radioactive particles in the reticuloendothelial cells of the liver, spleen, and bone marrow, and there is deposition on bone surfaces. [Pg.53]

Flavonoids in general are extensively metabolized by enterocyte and hepatic cell enzymes and by intestinal microflora. Therefore, it is necessary to explore the biological activity of flavonoids and their metabolites in specific tissues, because the metabolites found in the blood flow or any specific organ may differ among themselves and from... [Pg.168]

Fitzhugh and Nelson (19) found that oxalic acid up to 1.2% of the diet did not affect growth or mortality rate of rats fed oxalic acid for 1 year. Microscopic pathological examination showed no major visceral damage, but some of the rats showed slight periportal hypertrophy of the hepatic cells along with slight centrolobular atrophy. [Pg.109]

F) Hepatic 0.025 0.05 (hepatic cell vacuolation, slightly increased liver weights) ... [Pg.45]

Hassoun et al. (1993) examined the effects of various pesticides on lipid peroxidation and DNA single strand breakage in the hepatic cells of female Sprague-Dawley rats. Animals were dosed orally once with endrin at 4.5 mg/kg, lindane at 30 mg/kg, chlordane at 120 mg/kg, or DDT (dichlorodiphenyl trichloro-ethane) at 40 mg/kg, or vehicle only (com oil, control). At 6, 12, and 24 hours post-dosing, 4 animals from each group were sacrificed, their livers removed, and prepared for lipid peroxidation assay. Lipid peroxidation was measured calorimetrically by determining the amount of thiobarbituric acid reactive substances (TBARS) formed. Exposure to endrin resulted in a 14.5% increase in hepatic mitochondrial... [Pg.53]

The chronic oral MRL was based on a NOAEL of 0.025 mg/kg/day for convulsions in dogs administered endrin in the diet for 2 years (Kettering 1969). Concentrations of 0.05 and 0.1 mg/kg/day were associated with convulsive activity, slight to moderate vacuolization of hepatic cells, and occasional slight increases in liver weights. Other studies have reported hepatotoxicity in animals treated orally with endrin (Hassan etal. 1991 Treon et al. 1955). [Pg.76]

Kostner investigated the affinity of Lp(a) to hepatic cells (HepG2 and Hep3B) and detected an increased affinity of the LDL-receptor to LDL after incubation with apo(a) or Lp(a). Co-incubation with LDL caused a significant increase of Lp(a) degradation by HepG2 cells in a hitch-hike like process (K31). [Pg.90]

Pereira (1994) provided further evidence of the effect of dosing method (gavage versus drinking water) and vehicle (com oil versus water) on hepatic cell proliferation in female B6C3Fi mice. Animals received either 263 mg/kg/day chloroform by gavage in com oil or 1,800 ppm chloroform in drinking water,... [Pg.91]

The second thing that happens is a very good thing. The liver upregulates its LDL receptor level. In snm, the liver does the two things that it can do to maintain an adequate source of its cholesterol pump up the synthesis (to normal or slightly subnormal rates only) and pnmp np the seqnestration of cholesterol from the blood LDLs. The net effect is that the rate of excretion of cholesterol from the body is increased due to the increase in the nnmber of LDL receptors expressed on hepatic cells without compromising the availability of cholesterol to meet cellular needs. [Pg.270]

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