Liver 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). 

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... 

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. 

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. 

Although many animal models for iron overload exist, some mimicking certain aspects of HH, the 32-microglobulin knockout mouse is of special interest as it revealed for the first time crucial aspects of the pathogenesis of human HH in an animal model, and also because it underlines the important links between iron metabolism and the immune system. Hepatic iron overload in 32-microglobulin ( 32m)-deficient mice appeared to be similar to that found in HH, with pathological iron depositions occurring predominantly in liver parenchymal cells (de Sousa et ah,... 

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. 

Bellemann, P. (1980). Primary monolayer culture of liver parenchymal cells and kidney cortical tubules as a useful new model for biochemical pharmacology and experimental toxicology. Studies in vitro on hepatic membrane transport, induction of liver enzymes, and adaptive changes in renal cortical enzymes. Arch. Toxicol. 44 63-84. 

F) Hepatic 0.025 0.05 (hepatic cell vacuolation, slightly increased liver weights) ... 

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... 

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). 

The over-production of bilirubin to the point at which the liver s capacity to metabolize is exceeded or if there is dysfunction of the liver itself due to damage or metabolic immaturity, can lead to a yellow discolouration of tissues called jaundice. The accumulation of unconjugated bilirubin in neonates, often as a result of antibody-mediated destruction of the baby s red cells is dangerous as serious and irreversible brain damage can occur. Acute or chronic damage to the adult liver (hepatitis) may cause jaundice but not brain damage. 

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. 

Eongere Deschatrette C, Imaizumi-Scherrer T, Strick-Marchand H, Morosan S, Charnean P, Kremsdorf D et al (2006). Plasticity of hepatic cell differentiation bipotential adult mouse liver clonal cell lines competent to differentiate in vitro and in vivo. Stern Cells 24 2098 2109. 

The use of the reticulo-endothelial system (RES) was the first approach to liver contrast agents. As an adjunct, spleen imaging would also be possible with a contrast agent that is taken up by the RES. The Kupffer cells of the liver, which represent 10% of all hepatic cells, constitute the major portion (80-90%) of all fixed macrophages and they are extremely effective in the phagocytosis of all types of particles. The downside of the use of this mechanism, however, is the concomitant release of toxic mediators that might and - as a matter of fact - often has made this approach non-feasible. Adverse events provoked by the mediators are changes in blood pressure (most often hypotension) and fever. 

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