• Preventive Nutrition and Food Science
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• v.2 no.1
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• pp.35-41
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• 1997

The pancreas is an important organ in the maintenance of zinc homeostasis. Endogenous zinc is con-tinuously secreted via pancreatic exocrine fluid or to a lesser extent in bile. Much of the endogenous secretion must be reabsorbed to sustain zinc homeostasis. The objective of this study was to estimate the relative size of the pancreatic/biliary zinc pool in comparision to the dietary zinc intake, and to study the effect of the phytate and calcium on the zinc homeostasis using a rat model. At the termination of the experiment, pan-creatic/biliary fluid was collected from the rats. Both radioactivity and total zinc were measured and the relative size of the pancreatic/biliary zinc pool was estimated. To determine the effect of phytate and calcium on zinc homeostsis, dietary zinc intake, the amount of zinc in pancreatic.biliary fluid and fecal zinc excretion were measured. The flow rate of pancreatic/biliary fluid, as corrected for tubing constriction, gives the corrected zinc concentration in the pancreatic/biliary fluid was 2.2 times higher than dietary zinc intake. To maintain zinc homeostasis, zinc absorption/reabsorption was very efficient in the current model; 76%, 88% of absorption/reabsorption for low calcium group and high calcium group 81% for phytate group and non-phytate group, respectively.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.4
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• pp.387-397
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• 2016

Neurofibrillary tangles (NFTs) of microtubule-associated protein tau are a pathological hallmark of Alzheimer's disease (AD). Endoplasmic reticulum (ER) stress has been known to be involved in the pathogenesis of AD. However, the exact role of ER stress in tau pathology has not yet been clearly elucidated. In present study, the possible relationship between tau pathology and ER stress was examined in terms of sorcin, which is a calcium binding protein and plays an important role in calcium homeostasis. Our previous yeast two hybrid study showed that sorcin is a novel tau interacting protein. Caspase-3-cleaved tau (T4C3) showed significantly increased tau-sorcin interaction compared to wild type tau (T4). Thapsigargin-induced ER stress and co-expression of constitutively active $GSK3{\beta}$ ($GSK3{\beta}-S9A$) also exhibited significantly increased tau-sorcin interactions. T4C3-expressing cells showed potentiated thapsigargin -induced apoptosis and disruption of intracellular calcium homeostasis compared to T4-expressing cells. Overexpression of sorcin significantly attenuated thapsigargin-induced apoptosis and disruption of calcium homeostasis. In contrary, siRNA-mediated knock-down of sorcin showed significantly increased thapsigargin-induced apoptosis and disruption of calcium homeostasis. These data strongly suggest that sequestration of sorcin by aberrant forms of tau compromises the function of sorcin, such as calcium homeostasis and cellular resistance by ER stress, which may consequently result in the contribution to the progression of AD.

• Clinical and Experimental Pediatrics
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• v.50 no.3
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• pp.230-235
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• 2007

In the early neonatal period, the neonate is challenged by the loss of the placental calcium transport and manifests a quick transition, from an environment in which PTHrP plays an important role to a PTH- and 1,25-dihydroxyvitamin D-controlled neonatal milieu. Disturbances in mineral homeostasis are common in the neonatal period, especially in premature infants and infants who are hospitalized in an intensive care unit. In many cases these disturbances are thought to be exaggerated responses to the normal physiological transition from the intrauterine environment to neonatal independence. Some disturbances in calcium and phosphate homeostasis are the result of genetic defects, which in many instances can now be identified at the molecular level. Although fetus develop remarkably normally in the presence of maternal calcium, PTH and vitamin D deficiency, the neonates demonstrate abnormalities that are consequences of the prior abnormal maternal calcium homeostasis. Evaluation and management of hypocalcemia and hypercalcemia in neonate requires specific knowledge of perinatal mineral physiology and the unique clinical and biochemical features of newborn mineral metabolism.

• Toxicological Research
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• v.20 no.3
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• pp.241-250
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• 2004

We previously found that bisphenol A (BPA) caused neurotoxic behavioral alteration. Since disturbance of calcium homeostasis is an implicated contributor in the neurotoxic mechanism of environmental toxicants, we investigated whether BPA alters calcium homeostasis. Unlike other neurotoxic agents which cause increase of intracellular calcium level, BPA decreased $[Ca^{2+}]_i$ dose-dependently in PC12 cells and cortical neuronal cells regardless of the calcium existence in buffer. BPA at greater concentrations than 100 $\mu\textrm{M}$ reduced cell viability significantly in both types of cells. BPA also suppressed L-glutamate (L-type channel activator, 30 mM) and trifluoperazine (calmodulin antagonist, 30 $\mu\textrm{M}$)-induced increase of $[Ca^{2+}]_i$. BPA further lowered caffeine (RYR activator, 100 $\mu\textrm{M}$)-decreased $[Ca^{2+}]_i$, but did not alter dantrolene (RYR inhibitor, 100 $\mu\textrm{M}$), heparin (IP3 inhibitor, 200 units/ml) and xestospongin C (IP3 inhibitor, 5 $\mu\textrm{M}$)-decreased $[Ca^{2+}]_i$. Cell viability was not directly related to intracellular calcium change by bisphenol A that alternation of intracellular calcium may not be a direct causal factor of BPA-induced neuronal cell death.

• Asian-Australasian Journal of Animal Sciences
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• v.5 no.2
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• pp.303-308
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• 1992

Three female sheep were daily administered a pyrophosphate analogue, disodium 1-hydroxyethylidene-1, 1-bisphosphonate (HEBP) at the level of 4 mg/kg body weight. HEBP largely suppressed bone resorption, which was indicated by the reduction in plasma free hydroxyproline concentration and in calcium mobilization rate during the intravenous infusion of disodium ethylenediaminetetraacetate (EDTA). Contrary to the suppression of bone resorption, plasma total-calcium, magnesium and phosphorus concentrations were not changed by HEBP administration. These results suggest that bone mineral crystals play a meaningless role on calcium, magnesium and phosphorus homeostasis in ruminants if they are fed adequate amounts of these minerals. Plasma magnesium and phosphorus concentrations were not significantly changed after feeding. However, plasma total-calcium was decreased after feeding in both periods and the reduction seemed to be remarkable in the HEBP-treated period. Infusion of EDTA more remarkably reduced plasma ionized calcium concentration in the HEBP-treated that in the untreated period and the recovery of ionized calcium was retarded by HEBP administration. These results suggest that calcium release from bone is necessary for maintenance of plasma calcium when animals rapidly lose calcium.

• Asian Pacific Journal of Cancer Prevention
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• v.13 no.8
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• pp.3561-3568
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• 2012

The calcium sensing receptor (CaSR) is a member of the largest family of cell surface receptors, the G protein-coupled receptors involved in calcium homeostasis. The role of the CaSR in neoplasia appears to be homeostatic; loss of normal CaSR-induced response to extracellular calcium is observed in cancers of the colon and ovary, while increased release of PTHrP is observed in cancers of the breast, prostate and Leydig cells. Currently CaSR can be considered as a molecule that can either promote or prevent tumor growth depending on the type of cancer. Therefore, recognition of the multifaceted role of CaSR in gliomas and other malignant tumors in general is fundamental to elucidating the mechanisms of tumor progression and the development of novel therapeutic agents. Emphasis should be placed on development of drug-targeting methods to modulate CaSR activity in cancer cells.

• Biomolecules & Therapeutics
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• v.17 no.2
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• pp.125-132
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• 2009

Calbindin-$D_{9k}$ (CaBP-9k), a cytosolic calcium-binding protein, is expressed in a variety of tissues, i.e., the duodenum, uterus, placenta, kidney and pituitary gland. Duodenal CaBP-9k is involved in intestinal calcium absorption, and is regulated at transcriptional and post-transcriptional levels by 1,25-dihydroxyvitamin D3, the hormonal form of vitamin D, and glucocorticoids (GCs). Uterine CaBP-9k has been implicated in the regulation of myometrial action(s) through modulation of intracellular calcium, and steroid hormones appear to be the main regulators in its uterine and placental regulation. Because phenotypes of CaBP-9k-null mice appear to be normal, other calcium-transporter genes may compensate for its gene deletion and physiological function in knockout mice. Previous studies indicate that CaBP-9k may be controlled in a tissue-specific fashion. In this review, we summarize the current information on calcium homeostasis related to CaBP-9k gene regulation by GCs, vitamin D and its receptors, and its molecular regulatory mechanism. In addition, we present related data from our current research.

• Journal of Embryo Transfer
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• v.24 no.4
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• pp.237-247
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• 2009

Melatonin (N-acetyl-5-methoxytryptamine) is the major neurohormone secreted during the night by the vertebrate pineal gland. The circadian pattern of pineal melatonin secretion is related to the biological clock within the suprachiasmatic nucleus (SCN) of the hypothalamus in mammals. The SCN coordinates the body's rhythms to the environmental light-dark cycle in response to light perceived by the retina, which acts mainly on retinal ganglion cells that contain the photopigment melanopsin. Calbindin-D9k (CaBP-9k) is a member of the S100 family of intracellular calcium- binding proteins, and in this review, we discuss the involvement of melatonin and CaBP-9k with respect to calcium homeostasis and apoptotic cell death. In future studies, we hope to provide important information on the roles played by CaBP-9k in cell signal transduction, cell proliferation, and $Ca^{2+}$ homeostasis in vivo and in vitro.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.94.3-95
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• 2003

Familial form of Alzheimer's disease (FAD) is caused by mutations in presenilin-l (PS-1) and presenilin-2 (PS-2). PS1 and PS2 mutation are known to similar effects on the production of amyloid peptide (A ) and cause of neuronal cell dath in the brain of patient of Alzheimer's disease. The importance of the alternation of cellular calcium homeostasis in the neuronal cell death by PS1 mutation in a variety of experimental systems has been demonstrated. However, no studies on the effect of PS2 of mutant PS2 on cellular calcium homeostasis, and relevance of its change to neuronal cell vulnerability against neurotoxins have been reported. (omitted)

• Journal of Korean Neurosurgical Society
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• v.45 no.4
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• pp.231-235
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• 2009

Objective : While many factors contribute to aging, changes in calcium homeostasis and calcium related neuronal processes are likely to be important. High intracellular calcium is toxic to cells and alterations in calcium homeostasis are associated with changes in calcium-binding proteins, which confine free $Ca^{2+}$. We therefore assayed the expression of the calcium binding proteins calretinin and calbindin in the central auditory nervous system of rats. Methods : Using antibodies to calretinin and calbindin, we assayed their expression in the cochlear nucleus, superior olivary nucleus, inferior colliculus, medial geniculate body and auditory cortex of young (4 months old) and aged (24 months old) rats. Results : Calretinin and calbindin staining intensity in neurons of the cochlear nucleus was significantly higher in aged than in young rats (p<0.05) The number and staining intensity of calretinin-positive neurons in the inferior colliculus, and of calbindin-positive neurons in the superior olivary nucleus were greater in aged than in young rats (p<0.05). Conclusion : These results suggest that auditory processing is altered during aging, which may be due to increased intracellular $Ca^{2+}$ concentration, consequently leading to increased immunoreactivity toward calcium-binding proteins.