Calcium inositol phosphate effects

Selected entries from Methods in Enzymology [vol, page(s)] Chelation, 238, 74, 76, 297 buffers [for analysis of exocytosis, 221, 132 preparation, 219, 186 modulation of cytosolic buffering capacity with quin2, 221, 159] fluorescence assay, 240, 724-725, 740-742 fluorescence imaging, 225, 531 238, 303-304, 322-325, 334-335 free intracellular levels after bacterial invasion, 236, 482-489 free calcium in solutions for membrane fusion analysis, calculation and control, 221, 149 homeostasis mechanisms, 238, 80 hormonal elevation, 238, 79 inositol phosphate effect on release, 238, 207 determination of cytosolic levels [computer methods, 238, 73-75 with fura-2, 238, 73, 146 with indo-1, 238, 298, 316-317 with quin-2, 238, 297] hormone effects, 238, 79 ionomycin effects, 238, 79 membrane depolarization effects,... 

From the evidence accumulated so far, it seems likely that the cAMP signal transduction pathway will be a major effector of a stimulatory signal to the pars tuberalis, which can be regulated by melatonin [115]. The effect of aluminum as AlF41 has been studied on inositol phosphate accumulation, calcium mobilization, and cyclic AMP production in ovine pars tuberalis cells [116]. In the presence of 10 mmol L-1 LiCl, AlF41 stimulated the net accumulation of inositol phosphates over a 40-min incubation. Lithium is a known inhibitor of phosphatases in the inositol phosphate-recycling pathway. The results show the existence of a lithium-sensitive phosphoinositide signaling. 

The following effects take place because the receptors are coupled to adenylyl cyclase or to phospholipase C. Adenylyl cydase catalyzes the synthesis of cAMP, while phospholipase C catalyzes the hydrolysis of the phosphahdy -4,5-bisphos-phate, releasing inositol-1,4,5-trisphosphate (11 3). This IP3, in turn, travels to the endoplasmic reticulum, where it provokes the momentary release of calcium ions. The increase in ion levels, in turn, provokes activation of a number of protein kinases, as discussed in the Calcium and Phosphate seebon. All of these receptors are p(dypeptides that weave seven times in or out of the plasma membrane. All of these receptors are directly linked to G protein, and require G protein for transmitting their message within the membrane to various enzymes. 

Mepacrine inhibits phospholipase A2 and subsequently leukotrienes, which are calcium ionophores. Mepacrine also has an inhibitory effect on phospholipase C and subsequent inositol phosphate formation, which mobilizes cjdosolic calcium from intracellular stores. It has therefore been suggested that this might influence myocardial contractile function (SEDA-13, 241). However, mepa-crine is not cardiotoxic, although problems could arise in the presence of a sick myocardium. 

Little is known of the intracellular events involved in the augmentation of cyclic AMP accumulation elicited by H, -receptors in mammalian brain slices. However, it seems certain that another second messenger is involved, since the effect is not observed in membrane preparations [81, 205]. Calcium appears to be important for the response, since removal of external calcium reduces H,-receptor-mediated cyclic AMP accumulation in guinea-pig cerebral cortical slices [206]. Inositol phospholipid breakdown or its products (inositol trisphosphate and diacylglycerol) may also be involved, since H,-receptor stimulation is accompanied by an accumulation of inositol phosphates in slices of guinea-pig cerebral cortex [60, 207, 208]. Inositol trisphosphate may then... 

Studies in slices of rat cerebral cortex have shown that the accumulation of [3H]inositol 1-phosphate elicited by histamine can be abolished by omission of calcium from the incubation medium [240]. This is not the result that would be expected if inositol phosphate were generated solely by the pathway outlined in Figure 2.13 and does not support the hypothesis that phospholipase-C-mediated inositol phosphate production precedes, rather than results from, Ca2 + mobilization. However, interpretation of this finding is complicated by the effect of calcium ion removal on the incorporation of [3H]inositol into the... 

Orotic acid in the diet (usually at a concentration of 1 per cent) can induce a deficiency of adenine and pyridine nucleotides in rat liver (but not in mouse or chick liver). The consequence is to inhibit secretion of lipoprotein into the blood, followed by the depression of plasma lipids, then in the accumulation of triglycerides and cholesterol in the liver (fatty liver) [141 — 161], This effect is not prevented by folic acid, vitamin B12, choline, methionine or inositol [141, 144], but can be prevented or rapidly reversed by the addition of a small amount of adenine to the diets [146, 147, 149, 152, 162]. The action of orotic acid can also be inhibited by calcium lactate in combination with lactose [163]. It was originally believed that the adenine deficiency produced by orotic acid was caused by an inhibition of the reaction of PRPP with glutamine in the de novo purine synthesis, since large amounts of PRPP are utilized for the conversion of orotic acid to uridine-5 -phosphate. However, incorporation studies of glycine-1- C in livers of orotic acid-fed rats revealed that the inhibition is caused rather by a depletion of the PRPP available for reaction with glutamine than by an effect on the condensation itself [160]. 

Certain ions, e.g., oxalate and phosphate, can bind Ca within the intestinal canal and high intake of phosphate can restrict calcium absorption. A similar effect is encountered by phytic acid (inositol hexaphosphate) that is present in high amounts in certain cereals. Disturbances in the fat absorption (dietary) decreases the calcium absorption because Ca is bound to nonabsorbable fatty acids. 

Certain foods such as unrefined cereals and sugar cane juice contain organic phosphates, e.g. phytate (inositol hexaphosphate), which reduce enamel solubility, apparently by reacting with calcium phosphate salts on the enamel surface. The view that this type of compound has a caries-inhibiting effect is supported by observations that dietary supplements of calcium glycerophosphate reduce caries in rats and monkeys. At the same time, the calcium-binding properties of phytate may adversely affect the absorption of calcium from the intestine (page 143). 

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