Calcium cellular membranes, interaction with

There is a delicate balance between cellular membrane permeability and intracellular calcium homeostasis during CVB3 infection. It has been well-documented that sustained elevation of calcium levels in the cytosol precedes Cyt c release from the mitochondria, and that the small amount of released Cyt c interacts with the inositol triphosphate receptor (IP3R) on the endoplasmic reticulum (ER) and prevents inhibition of ER calcium release. The overall increase of calcium leads to a massive release of Cyt c to maintain ER calcium release through interaction with the IP3Rs in a positive feedback loop, and to activate downstream caspases to execute apoptosis of damaged cells. 

The precise mechanism by which NO causes glutamase neurotoxicity is unknown. Calcium must be required because of the requirement for NMDA- and glutamate-induced NO formation in brain tissue (Garthwaite etal., 1988). Although both NMDA-receptor agonists and sodium nitroprusside induce specific neurotoxicity as well as cyclic GMP formation in brain tissue (Dawson et al., 1991), it is unlikely that cyclic GMP is the ultimate cause of the neurotoxicity. Instead, NO is most likely involved in producing target cell death. One possible mechanistic pathway is that locally synthesized NO and superoxide anion react with each other to yield peroxynitrite anion (Beckman et al., 1990), which can destroy cell membranes either directly via interaction with cellular thiols (Radi et al., 1991) or indirectly via decomposition to hydroxyl and other free radicals (Beckman et al., 1990). 

As described in Chapter 4, regulatory G proteins act as an intermediate link between receptor activation and the intracellular effector mechanism that ultimately causes a change in cellular activity. In the case of opioid receptors, these G proteins interact with three primary cellular effectors calcium channels, potassium channels, and the adenyl cyclase enzyme.27 At the presynaptic terminal, stimulation of opioid receptors activates G proteins that in turn inhibit the opening of calcium channels on the nerve membrane.65 Decreased calcium entry into the presynaptic terminal causes decreased neurotransmitter release because calcium influx mediates transmitter release at a chemical synapse. At the postsynaptic neuron, opioid receptors are linked via G proteins to potassium channels, and... 

The deposition of mineral on one side of a cell membrane is affected by both the availability of calcium and carbonate ions and also by their interaction with other ions. Interfering ions not only impede the effective collisions of calcium and carbonate but they may also form ion pairs with the calcium and carbonate ions (Skirrow, 1975). Mg " and PO " may also interfere with the growth of the crystJil lattice so that, in their presence, the rate of calcification may be reduced and a particular crystal type may be favoured (Kitano et al., 1976). One of the functions of cellular membranes is probably to control the ionic composition of invertebrate skeletons and that of some intracellular mineral deposits. 

Skin tumor promoters bring about a number of other important epigenetic changes in the skin such as membrane and differentiation alterations and an increase in protease activity, cAMP independent protein kinase activity and phospholipid synthesis (.31). In addition, the skin tumor promoters cause a decrease in epidermal superoxide dismutase and catalase activities as well as a decrease in the number of glucocorticoid receptors (.31). Some skin promoters appear to have a common mode of cellular action - via binding to the natural cellular substrate for diacylglycerol-a phospholipid, calcium-dependent kinase called protein kinase C. Promoters which interact with protein kinase C include 12-H-tetradecanoylphorbol-... 

A. The multisystem toxicity of lead is mediated by several mechanisms, including inactivation or alteration of enzymes and other macromolecules by binding to sulfhydryl, phosphate, or carboxyl ligands, and interaction with essential cations, most notably calcium, zinc, and iron. Pathological alterations in cellular and mitochondrial membranes, neurotransmitter synthesis and function, heme synthesis, cellular redox status, and nucleotide metabolism may occur. Adverse impacts on the nervous, renal, hematopoietic, reproductive, and cardiovascular systems can result. 

From what we have seen in the preceding chapter, arachidonic acid meets at least two of these criteria like classical second messengers, e.g., cyclic AMP or inositoltrisphosphate, the cellular amounts of free arachidonate are finely tuned by a balance between receptor-dependent formation and enzymatic disposition. The question we need to address now is whether free arachidonate can transduce the actions of extracellular messenger molecules by interacting with intracellular target proteins. In the present chapter, I shall describe two circumstances in which non-esterified arachidonate has been shown to modulate protein functions directly, i.e., without undergoing further metabolism these are the regulation of membrane ion channels and the stimulation of the calcium- and phospholipid-dependent protein kinase, PKC. 

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