Membrane-proximal calcium

Omann, G.M., and Axehod, D. (1996). Membrane-proximal calcium transients in stimulated neutrophils detected by total internal reflection fluorescence. Biophys. J. 71, 2885-2891. 

Jaiswal JK, Andrews NW, Simon SM. 2002. Membrane proximal lysosomes are the major vesicles responsible for calcium-dependent exocytosis in non-secretory cells. J Cell Biol 159 625-635. 

The lipid in muscle is composed primarily of triglycerides (depot fats) and of phospholipids (membrane components), and is a constituent which varies enormously not only in amount present, but also in properties such as degree of saturation (species dependent). The ash of lean meat is comprised of various minerals such as phosphorus, potassium, sodium, magnesium, calcium, iron and zinc Carbohydrate was not noted in the proximate composition because while some may be present, it is normally there in low concentration compared to the other constituents. Glycogen is the carbohydrate occurring in greatest concentration in muscle but is normally degraded soon after the animal is sacrificed. 

Foscarnet competitively inhibits Na -Pj cotransport in animal and human kidney proximal tubule brush border membrane vesicles, reversibly inhibiting sodium-dependent phosphate transport [48, 49]. Renal cortical Na-K-ATPase and alkaline phosphatase activity are not inhibited by foscarnet, nor is proline, glucose, succinate, or Na" transport [48,49]. Foscarnet induces isolated phosphaturia without hypophosphatemia in thyroparathyroidectomized rats maintained on a low phosphorus diet, without affecting glomerular filtration rate, urinary adenosine 3 5 -cyclic monophosphate (cAMP) activity, or urinary calcium, sodium or potassium excretion [48,50]. Sodium-Pj cotransport in brush border membrane vesicles from human renal cortex was reported to be even more sensitive to inhibition by foscarnet than in rat renal brush border membrane vesicles [49]. 

For many years, acute administration of either Hg or Hg has been known to produce necrosis of the third segment of the proximal tubule [78-84]. The mechanisms that lead to these effects appear to involve alterations in intracellular calcium concentrations secondary to membrane damage. The mechanisms of Hg toxicity to renal tubule cells has been studied at the molecular level. Tarabova et al [85] reported that Hg ... 

The mechanism of proximal tubule toxicity following administration of mercuric chloride has been extensively studied. However, the key sequence of events leading to cell death remains to be determined with certainty. Mercuric ions induce mitochondrial toxicity, alter cell membrane function, disrupt cell calcium homeostasis and cause changes in membrane phospholipid composition. Binding of mercuric ions to enzymatic sulfhydryl groups and ischemia-induced mitochondrial toxicity have been proposed as the basic mechanisms leading to these cellular effects and ultimately to cell death. 

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