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Calcium homoeostasis

J. Benters, U. Flogel, T. Schafer, D. Leibfritz, S. Hechtenberg, D. Beyersmann, Study of the interactions of cadmium and zinc ions with cellular calcium homoeostasis using F-19-NMR spectroscopy, Biochem. J. 322 (1997) 793-799. [Pg.270]

O Rourke, F. A., LaPlante, J. M. and Feinstein, M. B., 2003, Antisense-mediated loss of calcium homoeostasis endoplasmic reticulum protein (CHERP ERPROT213-21) impairs Ca2+ mobilization, nuclear factor of activated T-cells (NFAT) activation and cell proliferation in Jurkat T-lymphocytes. Biochem J 373, 133-43. [Pg.425]

The progressive course of cell damage through to cell death is mainly characterized by two biochemical metabolic processes (1.) oxidative stress and (2.) disruption of intracellular Ca homoeostasis. These two processes interact, so that the oxidative stress induces the disruption of calcium homoeostasis there are also, however, other reciprocal actions/effects involving further cellular metabolic processes. (27)... [Pg.401]

Disrupted calcium homoeostasis Normal concentrations of ionized calcium in the cytosol (0.05-0.2 pM), in the overall liver cell (0.5-2.0 pM) and in the extracellular space (1.0 pM) maintain the function of numerous Ca-dependent enzymes and structural elements of the liver cell. Calcium homoeostasis is maintained by the regulatory functioning of all Ca transportation systems, energy supply in the form of ATP and intactness of the biomembranes. Defective calcium homoeostasis can cause an increase in calcium in the cytosol, which in turn activates calcium-dependent enzymes, alters the metabolic functions of the cell and disrupts the gap junctions and tight junctions. These biochemical changes result in various forms of hepatocellular degeneration and ultimately in cell death, (s. fig. 21.12)... [Pg.402]

Fig. 21.12 Biochemical causative mechanisms of hepatocellular degeneration and cell death due to oxidative stress and disruptions of cellular calcium homoeostasis (similar to a vicious circle)... Fig. 21.12 Biochemical causative mechanisms of hepatocellular degeneration and cell death due to oxidative stress and disruptions of cellular calcium homoeostasis (similar to a vicious circle)...
Bone is a dense specialized form of connective tissue with mechanical (skeleton provides rigidity functioning as attachment and lever for ligaments and musculature), chemical (calcium homoeostasis and metabolism), and hematological functions. Cortical (also called compact bone) and trabecular (also known as spongy or cancellous bone) are the two main types of bone. Cortical bone is denser, less porous, and less studied with MR than trabecular bone. Cortical bone forms the shaft of long bones and the covering around trabecular bone at the end of joints and the vertebrae. Trabecular bone is made up of an intricate porous network of tiny strands and thin plates of bone called trabeculae. It... [Pg.283]

Bishop NJ, et al. Changes in calcium homoeostasis in patients undergoing liver transplantation Effects of a single infusion of pamidronate administered pre-operatively. ChnSci(Lond) 1999 97 157-163. [Pg.2657]

The second level involves two kinds of cellular participation resorption of existing bone by osteoclasts and deposition of new bone by osteoblasts. Over short periods these two processes, acting at different sites, approximately balance each other. Acting in conjunction, they not only continuously remodel the surface contour of the bone but also play a major part in the control of calcium and phosphorus metabolism for the whole organism. Coordination at this second level is achieved through hormonal mediation of calcium and phosphate homoeostasis which ensures that the concentrations of these ions in the plasma and tissue fluid remain constant (Chapter 30). [Pg.436]

A more positive control of calcium ion concentration is brought about by the cell-mediated resorption or deposition of stable bone material. These adjustments are slower, but quantitatively greater, than the simple exchange reaction. They take place with great precision with regard to the sites in the bone where resorption and deposition occur, their timing and the constancy of plasma ion concentration achieved. The process thus provides for both the continuous remodelling of bone and for the calcium-phosphorus homoeostasis of the blood and tissue fluids. The former depends on the position on the bone surface of various stimulated cells and the latter on the net result of stimulation of cells in bone, intestine and kidney by parathyroid hormone, calcitonin and vitamin D. The mode of action of these substances and the interplay of their various effects are complex. [Pg.448]


See other pages where Calcium homoeostasis is mentioned: [Pg.417]    [Pg.827]    [Pg.472]    [Pg.417]    [Pg.827]    [Pg.472]    [Pg.330]    [Pg.436]    [Pg.448]    [Pg.449]    [Pg.451]    [Pg.267]   
See also in sourсe #XX -- [ Pg.402 ]




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Homoeostasis

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