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Parenchymal cell

Smooth muscle cells constitute the most diversified class of muscle cells. They are the parenchymal cells of many organs, including the uterus and other reproductive organs, gall bladder, urinary bladder, respiratory passages, etc. In all these cases,... [Pg.155]

Compartmentation of pathways in separate subcellular compartments or organelles permits integration and regulation of metabolism. Not all pathways are of equal importance in all cells. Figure 15-7 depicts the subceh lular compartmentation of metabohc pathways in a hepatic parenchymal cell. [Pg.126]

Figure 15-7. Intracellular location and overview of major metabolic pathways in a liver parenchymal cell. (AA —metabolism of one or more essential amino acids AA <->, metabolism of one or more nonessential amino acids.)... Figure 15-7. Intracellular location and overview of major metabolic pathways in a liver parenchymal cell. (AA —metabolism of one or more essential amino acids AA <->, metabolism of one or more nonessential amino acids.)...
There are striking similarities in the mechanisms of formation of chylomicrons by intestinal cells and of VLDL by hepatic parenchymal cells (Figure 25—2), perhaps because—apart from the mammary gland—the intestine and liver are the only tissues from which particulate lipid is secreted. Newly secreted or nascent chylomicrons and VLDL contain only a small amount of apolipoproteins C and E, and the frill complement is acquired from HDL in the circulation (Figures 25—3 and 25-4). Apo B is essential for chylomicron and VLDL formation. In abetalipoproteinemia (a rare disease), lipoproteins containing apo B are not formed and lipid droplets accumulate in the intestine and liver. [Pg.207]

Bilirubin formed in peripheral tissues is transported to the hver by plasma albumin. The further metabolism of bihtubin occuts primarily in the hver. It can be divided into thtee processes (1) uptake of bilirubin by hver parenchymal cells, (2) conjugation of bilirubin with glucuronate in the endoplasmic reticulum, and (3) secretion of conjugated bilirubin into the bile. Each of these processes will be considered separately. [Pg.280]

The commonest causes of obstructive (posthepatic) jaundice are cancer of the head of the pancreas and a gallstone lodged in the common bile duct. The presence of bilirubin in the urine is sometimes referred to as choluria—therefore, hepatitis and obstruction of the common bile duct cause choluric Jaundice, whereas the Jaundice of hemolytic anemia is referred to as acholuric. The laboratory results in patients with hepatitis are variable, depending on the extent of damage to parenchymal cells and the extent of micro-obstruction to bile ductules. Serum levels of ALT and AST are usually markedly elevated in hepatitis, whereas serum levels of alkaline phosphatase are elevated in obstructive liver disease. [Pg.284]

Reynolds, E.S. (1967). Liver parenchymal cell injury IV Pattern of incorporation of carbon and chlorine atoms from carbon tetrachloride into chemical constituents of liver in vivo. J. Pharmacol. Exp. Therap. 155, 117-126. [Pg.245]

Initiation Release of growth factors inflammatory cytokines by parenchymal cells... [Pg.421]

Researchers focused on the metabolically competent human hepatoma cell line HepG2 as a model of human liver. HepG2 cells are a well-known hepatoma cell line that retains many of the morphological characteristics of liver parenchymal cells. This model is often used as a useful tool for HRA/ERA-oriented chemical risk assessment due to the expression of antioxidant and xenobiotic metabolizing enzymes (in particular phase I and phase II enzymes responsible for the bioactivation/detoxification of various xenobiotics) that can be induced or inhibited by dietary and non-dietary agents [28-30]. [Pg.178]

Figure 8.1 Body iron stores and daily iron exchange. The figure shows a schematic representation of the routes of iron movement in normal adult male subjects. The plasma iron pool is about 4 mg (transferrin-bound iron and non-transferrin-bound iron), although the daily turnover is over 30 mg. The iron in parenchymal tissues is largely haem (in muscle) and ferritin/haemosiderin (in hepatic parenchymal cells). Dotted arrows represent iron loss through loss of epithelial cells in the gut or through blood loss. Numbers are in mg/day. Transferrin-Tf haemosiderin - hs MPS - mononuclear phagocytic system, including macrophages in spleen and Kupffer cells in liver. Figure 8.1 Body iron stores and daily iron exchange. The figure shows a schematic representation of the routes of iron movement in normal adult male subjects. The plasma iron pool is about 4 mg (transferrin-bound iron and non-transferrin-bound iron), although the daily turnover is over 30 mg. The iron in parenchymal tissues is largely haem (in muscle) and ferritin/haemosiderin (in hepatic parenchymal cells). Dotted arrows represent iron loss through loss of epithelial cells in the gut or through blood loss. Numbers are in mg/day. Transferrin-Tf haemosiderin - hs MPS - mononuclear phagocytic system, including macrophages in spleen and Kupffer cells in liver.
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,... [Pg.261]

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. [Pg.677]

Mesenchymal tissue is immature, unspecialized tissue, found in the early embryo of animals, whereas epithelial cells are parenchymal cells that line an internal cavity or tube. [Pg.336]

Reynolds ES, Yee AG. 1967. Liver parenchymal cell injury. V. Relationships between patterns of chloromethane-C14 incorporation into constituents of liver in vivo and cellular injury. Lab Invest 16 591-603. [Pg.283]

Finally the ion mnst leave the symplast of the xylem and be loaded into the xylem s long-distance conducting vessels. The mechanism of xylem loading apparently involves both passive and active transfer from the xylem parenchymal cells. [Pg.181]


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