Calcium uptake inhibition

Doherty, J.D., K. Nishimura, N. Kurihara, and T. Fujita. 1986. Quantitative structure-activity studies of substituted benzyl chrysanthemates. 9. Calcium uptake inhibition in crayfish nerve cord and lobster axon homogenates in vitro by synthetic pyrethroids. Pestic. Biochem. Physiol. 25 295-305. 

Nickel may be a factor in asbestos carcinogenicity. The presence of chromium and manganese in asbestos fibers may enhance the carcinogenicity of nickel (USEPA 1980), but this relation needs to be verified. Barium-nickel mixtures inhibit calcium uptake in rats, resulting in reduced growth (WHO 1991). Pretreatment of animals with cadmium enhanced the toxicity of nickel to the kidneys and liver (USPHS 1993). Simultaneous exposure to nickel and cadmium — an industrial situation... 

Doherty JD, Nishimura K, Kurihara N, Fujita T (1987) Promotion of norepinephrine release and inhibition of calcium uptake by pyrethroids in rat brain synaptosomes. Pestic Biochem Physiol 29 187-196... 

Mercuric chloride is thought to gain access to the intracellular compartment through Na + and Ca2 + channels in the membrane [ 100]. Sulphydryl reagents, including Hg2 +, could inhibit K +-stimulated uptake of Ca2+ into rat brain synaptosomes in vitro [101]. In muscle sarcoplasmic reticulum, Hg2+ causes inhibition of ATP-dependent Ca2 + uptake and loss of accumulated calcium [ 102,103]. However, HgCl2 has been found to inhibit ATP-dependent calcium uptake more strongly than it inhibits potassium-stimulated uptake [ 104],... 

At the cellular level, chlordecone causes spontaneous neurotransmitter release (End et al. 1981) and increases in free intracellular calcium in synaptosomes (Bondy and Halsall 1988 Bondy and McKee 1990 Bondy et al. 1989 Komulainen and Bondy 1987). This appears to be due at least in part to increased permeability of the plasma membrane (Bondy and Halsall 1988 Bondy and McKee 1990 Bondy et al. 1989 Komulainen and Bondy 1987), activation of voltage-dependent calcium channels (Komulainen and Bondy 1987), and inhibition of brain mitochondrial calcium uptake (End et al. 1979, 1981). 

Resorption of the required mineral substances from food usually depends on the body s requirements, and in several cases also on the composition of the diet. One example of dietary influence is calcium (see p. 342). Its resorption as Ca is promoted by lactate and citrate, but phosphate, oxalic acid, and phytol inhibit calcium uptake from food due to complex formation and the production of insoluble salts. 

Srivastava SP, Chen NQ, Floltzman JL. 1990. The in vitro NADPFI- dependent inhibition by CCFof the ATP-dependent calcium uptake of hepatic microsomes from male rats. J Biol Chem 265 8392-8399. 

Calcium ions are bound with an identical high affinity of 5.106M by the purified ATPase, by the transport protein in the native membranes as well as by partially deli-pidated, reversibly inactivated membrane preparations"8, ll9 173). The amount of calcium which is bound with that high affinity corresponds to two sites per transport molecule. The observed affinity is in good agreement with the affinity derived from the dependence on ionized calcium of the activation of calcium uptake and ATP splitting as well as of the inhibition of calcium release and ATP synthesis18 u2,, 74 17s Since the latter experiments were performed under conditions which provide a constant internal free calcium concentration by the presence of oxalate or phosphate in the system, the reactions must have been activated or inhibited by the calcium ions... 

Fig. 12. Activation of calcium uptake and the inhibition of calcium release and ATP synthesis by calcium ions. T calcium uptake, ----- calcium release, ---- ATP synthesis...

The calcium uptake process appears to involve exchange with H+. Thus the ionophore nigericin, which catalyzes an H+/K+ exchange, inhibits uptake of calcium in the presence of potassium. 

With the isolated perfused duodenum, there is a rapid increase in calcium transport in response to the addition of calcitriol to the perfusion medium. Isolated enterocytes and osteoblasts also show a rapid increase in calcium uptake in response to calcitriol. It is not associated with changes in mRNA or protein synthesis, but seems to be because of recruitment of membrane calcium transport proteins from intracellular vesicles to the cell surface. It is inhibited by the antimicrotubule compound colchicine. It can only be demonstrated in tissues from animals that are adequately supplied with vitamin D in vitamin D-deficient animals, the increase in intestinal calcium absorption occurs only more slowly, together with the induction of calbindin. 

Calcium channel blockers bind specifically to receptor sites associated with the voltage-dependent calcium channels [31,32]. These blockers inhibit calcium uptake [33,34] and block smooth muscle contraction [35,36]. All these three activities of calcium channel blockers have been found to be mutually correlated. For ten known calciiun channel blockers (Table 4), Papaionnou et al. [37] derived the correlations ... 

These ion movements are shown schematically in Figure 11. It should be noted that the orientation of the protonmotive force is reversed from that in vivo. The proton-pumping Mg -ATPase will be described in a later section. This calcium transport system is not inhibited significantly by ruthenium red, the classical inhibitor for calcium uptake in mitochondria. However, uptake of Ca by these inside-out vesicles of E. coli is inhibited dramatically by a dimeric, mixed-valence complex of Ru" ", [(NH3)3RuCl3Ru(NH3)3]. The mode of action remains to be established. 

BHC produces a variety of neurological effects in insects and mammals. However, at both levels of the nervous system (peripheral and central), the mechanism of toxic action of BHC is poorly understood. Central nervous system stimulation appears to be due to blockade of the effects of y-aminobutyric acid. In vitro BHC isomers are reported to increase the calcium uptake of isolated rat brain synaptosomes. In addition, y-isomer of BHC has been shown to inhibit... 

Summary - Many diverse novel compounds that inhibit different platelet functions show great promise, not only for potential anti-thrombotic agents, but also for more specific effects on prostaglandin and/or thromboxane A2 synthesis, and serotonin or calcium uptake and release. Many active compounds can be used as tools in the search toward a more complete understanding of the physiologic interactions of the hemostatic mechanisms. This better understanding would lead to the development and use of more potent and selective synthetic compounds in the inhibition of platelet aggregation and fibrin formation, and in the enhancement of fibrinolysis for the control of both arterial and venous thrombosis. It is hoped that some of these new compounds will be evaluated clinically in the near fu ture. 

An early report suggested that suramin can block the nucleotide-dependent calcium pump of rabbit skeletal sarcoplasmic reticulum by inhibition of the calcium uptake and the ATTase activity [51]. These results have been confirmed by Emmik et al. [52]. Baumert and Heider [53] found that pyridoxal-5-phosphate and a series of its analogues (for chemical structure. 

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