Transport calcium

The amount of each element required in daily dietary intake varies with the individual bioavailabihty of the mineral nutrient. BioavailabiUty depends both on body need as deterrnined by absorption and excretion patterns of the element and by general solubiUty, and on the absence of substances that may cause formation of iasoluble products, eg, calcium phosphate, Ca2(P0 2- some cases, additional requirements exist either for transport of substances or for uptake or binding. For example, calcium-binding proteias are iavolved ia calcium transport an intrinsic factor is needed for vitamin cobalt,... 

Vitamin D withdrawal is an obvious treatment for D toxicity (219). However, because of the 5—7 d half-life of plasma vitamin D and 20—30 d half-life of 25-hydroxy vitamin D, it may not be immediately successful. A prompt reduction in dietary calcium is also indicated to reduce hypercalcemia. Sodium phytate can aid in reducing intestinal calcium transport. Calcitonin glucagon and glucocorticoid therapy have also been reported to reduce semm calcium resulting from D intoxication (210). 

BAL—see Propan-l-ol, 2,3-dimercapto-Bacillus cereus calcium transport, 6,572 Bacillus megaterium calcium efflux, 6, 570 calcium transport, 6,572 sporulation zinc transport, 6, 572 Bacillus spp. sodium ions, 6, 559 sporulation... 

Nerve growth factor snake venoms zinc, 6, 613 Neurospora crassa calcium transport, 6, 571 cation transport, 6, 559 Neurosporin, 6, 676 Neurotransmitters secretion calcium, 6, 595 Neutral complexes electrical properties, 6, 143 Neutron absorbers... 

Pathogenesis of MH is not completely understood. Skeletal muscle, however, is the one tissue in MH with proven abnormalities, and it is further thought that the basic defect that causes the syndrome lies in the calcium regulation system found within the myoplasm. For example, calcium transport function appears to be decreased in the sarcoplasmic reticulum, mitochondria, and sarcolemma. Thus, the suggestion has been made that MH is characterized by a generalized membrane defeet. 

The toxic mechanism of action of these various jellyfish venoms is complex. The cardiotoxic reaction seems to focus on calcium transport and is blocked by the prior or post administration of therapeutic doses of verapamil (7J). In neuronal tissue, Chrysaora venom induces large cationic selective channels which open and close spontaneously. These channels are permeable to Na , Li, K, and Cs but not and the channels are present in spite of the treatment with sodium and potassium inhibitors such as tetrodotoxin and tetraethylammonium (14). 

ARJMANDI B H, KHALIL D A and HOLLIS B w (2000) Ipiiflavone, a synthetic phytoestrogen, enhances intestinal calcium transport in vitro. Calcif Tissue Int 67, 225-29. 

ARJMANDI B H, SALIH M A, HERBERT D c, SIMS s H and KALU D N (1993) Evidence for estrogen receptor-linked calcium transport in the intestine. Bone and Mineral 21, 63-74. 

S Muallem. (1989). Calcium transport pathways of pancreatic acinar cells. Annu Rev Physiol 51 83-105. 

Bronner F, Pansu S, Stein WD. 1986. An analysis of intestinal calcium transport across the rat intestine. Am J Physiol 250 G561-G569... 

Agarwal, A.K. and J.W. Coleman. 1988. Effect of paraquat on lung calcium transport. Toxicol. Lett. 42 317-323. 

Katz, A. M., Tada, M., and Kirchberger, M. A. (1975) Control of calcium transport in the myocardium by the cyclic AMP-protein kinase system. In Advances in Cyclic Nucleotide Research, Vol. 5, edited by G. 1. Drummond, P. Greengard, and G. A. Robinson, pp. 453-472. Raven Press, New York. 

Prenatal and postnatal exposures to fenvalerate reduced prostate and seminal vesicle weights and plasma testosterone levels in male rats [55], A chronic study showed no adverse effects on reproductive tissues at a high dose level of 1,000 ppm [142]. In vivo and in vitro studies with rats and mice suggested that fenvalerate may affect male and female reproduction, possibly due to calcium transport alteration [143-146], One paper reported that fenvalerate affected human sperm count and sperm motility of male workers who were exposed to fenvalerate in a pesticide factory [147]. 

Flik, G., Verbost, P. M. and Wendelaar Bonga, S. E. (1995). Calcium transport processes in fish. In Cellular and Molecular Approaches to Fish Ionic Regulation. eds. Wood, C. M. and Shuttleworth, T. J., Fish Physiology Series, Vol. 14, Academic Press, San Diego, pp. 317-342. 

From preliminary in vitro experiments using rat renal slices, it appears that the hormone directly affects renal calcium transport. If insulin is the mediator of the hypercalciuria, it might be possible to reduce urinary calcium loss by lowering the intake of in-sulinogenic foods. This would be especially important in those individuals with a marked calciuric response to such foods. 

We have tested the hypothesis that insulin inhibits the stimulatory effect of parathyroid hormone (PTH) on calcium reabsorption in the distal nephron. PTH is known to enhance calcium transport in renal cells, probably by stimulation of adenylate cyclase and subsequent increases in 3 5 cyclic AMP productoin. Since insulin had been observed to inhibit PTH-stimulated increases in kidney cyclic AMP levels in vitro (24) we investigated whether insulin-mediated hypercalciuria was dependent on the presence of PTH in vivo. 

As anticipated, arginine infusion caused a large (221 percent) increase in calcium excretion in sham-operated animals. Parathyroidectomy had no effect on the calciuric response to arginine uri-ary calcium increases in PTX control and arginine-infused animals were 299 and 302 percent respectively. These results persisted when data were corrected for differences in GFR. The data illustrate that neither PTH activity nor secretion is involved in insulin impairment of renal calcium transport. 

While our data using this technique are still preliminary, we have observed that 25 yU/ml insulin inhibits the rate of calcium efflux from renal slices (28). This effect of insulin was gradually reduced at the higher concentrations of insulin. The effects of insulin on calcium exchange appear to be localized in the mitochondrial compartment. Further work is needed to determine whether insulin affects specific enzyme systems which are known to play a role in renal calcium transport, and which cellular or subcellular compartments are involved. This would substantially increase our understanding of the regulation of urinary calcium excretion, and of ways in which excessive loss of calcium by this route might be avoided. 

End DW, Carchman RA, Ameen R, et al. 1979. Inhibition of rat brain mitochondrial calcium transport by chlordecone. Toxicol appl Pharmacol 51 189-196. 

Kodavanti PR, Cameron JA, Yallapragada PR, et al. 1990a. Effect of chlordecone (Kepone) on calcium transport mechanisms in rat heart sarcoplasn-dc reticulum. Pharinaeol Toxicol 67(3) 227-234. 

INTESTINE Characterization of a membrane potassium ion conductance in intestinal secretory cells using whole cell patch-clamp and calcium-sensitive dye techniques, 192, 309 isolation of intestinal epithelial cells and evaluation of transport functions, 192, 324 isolation of enterocyte membranes, 192, 341 established intestinal cell lines as model systems for electrolyte transport studies, 192, 354 sodium chloride transport pathways in intestinal membrane vesicles, 192, 389 advantages and limitations of vesicles for the characterization and the kinetic analysis of transport systems, 192, 409 isolation and reconstitution of the sodium-de-pendent glucose transporter, 192, 438 calcium transport by intestinal epithelial cell basolateral membrane, 192, 448 electrical measurements in large intestine (including cecum, colon, rectum), 192, 459... 

CalbindingK 3ICB 2.3 0.178 2 regulation Calcium transport Szebenyi and Moffat (1986, 1987)... 

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