• Journal of Nutrition and Health
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• v.30 no.4
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• pp.394-405
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• 1997

Endogenous zinc is important for maintaining zinc homeostasis because the size of endogenous zinc pool is almost 3-4 times bigger than that of dietary zinc. The purpose of this study was to examine the phytate effect on the reabsorption of endogenous zinc and the additional Ca effect on the phytate effect. Rats were fed a casein-based diet with added sodium phytate containing either high(1.6%) or low(0.8%) Ca concentrations for 4 weeks to reduce the body zinc pool. After the depletion period, $^{65}$ Zn was given by intraperitoneal injection to label the endogenous zinc pool. Rats were then assigned into phytate or non-phytate group within the same Ca group. feces were collected for 2 weeks of the initial collection period and 1 week after dietary crossover. The ratios of excreted fecal $^{65}$ Zn radioactivity of phytate group non-phytate group were determined as a measure of the phytate effect on the endogenous zinc. Mean fecal $^{65}$ Zn radioactivity was higher in the phytate group than in the non-phytate group during the entire 3 weeks of the collection period in the low Ca group, and during the initial collection period in the high Ca group(p <0.0001). This study showed an adverse phytate effect on endogenous zinc at both high and low dietary Ca levels. Elevated dietary Ca levels showed a synergistic effect on the phytate effect on endogenous zinc(p <0.05). These results imply greater phytate effect on zinc homeostasis rather than on zinc bioavailability through complexing with the endogenous zinc which is larger portion than the dietary zinc on zinc homeostasis.

• 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.

• Asian-Australasian Journal of Animal Sciences
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• v.14 no.2
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• pp.276-279
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• 2001

The effect of helminthiasis on zinc metabolism was monitored using endogenous $^{65}Zn$ after intraperitoneal injection of 1 g of $^{65}Zn$ as zinc chloride. In the first experiment zinc turnover was investigated in 18 male weanling rats, which were randomly divided into 3 groups. One group was infected with 73 third stage larvae of Nippostrongylus brasiliensis per gram body weight ; the other groups were the pair-fed and ad lib-fed controls. The route of loss of zinc was investigated in the second experiment with the same design using 18 animals with a lower dose of infection (33 larvae per gram body weight). The biological half life of endogenous $^{65}Zn$ was lower (p<0.05) in the infected group as compared to the controls. In the later phase of infection (9th to 16th day) there was reduced retention of $^{65}Zn$ and increased loss (p<0.05) of $^{65}Zn$ from the body though urine and faeces. It was concluded that infection of N. brasiliensis was accompanied by increased loss of endogenous Zn through faeces and urine.

• Journal of Nutrition and Health
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• v.30 no.4
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• pp.406-414
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• 1997

It has been known that dietary phytate decreases the absorption of body zinc pool which is composed of the dietary and endogenous zinc in the body. The purpose of this study was to examine the effect of phytate on the absorption of total bodyzinc in Zn-depleted rats. Rats were Zn-depleted with either low(0.8%) or high(1.6%) Ca diet containing sodium phytate for 4 weeks. After zinc depletion, rats were assigned into phytate or non-phytate dietary groups within each low-or high-Ca dietary group. ant feces were collected for 2 weeks of the initial collection and 1 week after dietary crossover, during which the phytate and the non-phytate diet was switched over within the same Ca group. The content of Zn and Ca measured by atomic absorption spectrophotometer and phytate content was analyzed. food intake was higher in the high Ca group than in the low Ca group(p <0.0001), and was also higher in the non-phytate group than in the phytate group(p <0.0001). Food intake and phytate level affected body weight gain in rats(p <0.0001). Zinc excretion in the total feces was higher in the phytate group than in the non-phytate group at both low and high Ca level(p <0.0001), except during the crossover collection period in high Ca group. Calcium, however, didn't show any synergistic effect on phytate effect(p <0.05). This study showed that phytate decreased the absorption of total body zinc at both low and high Ca levels in Zn-depleted rats. A large portion of total body zinc originated from the endogenous zinc pool in these rats. The results of the present study showed the same effect of phytate on the endogenous zinc in Zn-depleted rats as in a previous study, confirming that phytate adversely affects zinc bioavailability, especially under marginal and poor zinc nutrition.

• Proceedings of the Korean Nutrition Society Conference
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• 1995.11b
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• pp.61-61
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• 1995

• Journal of the Korean Society of Food Science and Nutrition
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• v.24 no.2
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• pp.346-353
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• 1995

The dietary requirement for zinc to maintain optimally the various metabolic and physiological funcitons is still under study. Human beings adapt to reductions in zinc intake by reducing the rate of growth or zinc excretion. Reductions in dietary zinc beyond the capacity to maintain homeostasis lead to utilization of zinc from an exchangeable pool. Loss of a small, critical amount of zinc from this pool leads to both biochemical and clinical signs of zinc deficiency. Zinc requirements have been assessed by balance studies and factorial method. As tissue zinc status influences endogenous losses and the dietary needs, individuls in good status may require higher amounts of zinc than those in poor status. While plasma zinc is insensitive to reducitons in dietary zinc, it is regarded as a valid, useful indicator of the exchangeable pool of zinc. Plasma metallothionein concentrations may prove useful for identifying poor zinc status. It has been suggested that functional end point measurement is the new direciton for zinc requirement. However, determination of the functional response to a marginal zinc intake is difficult because of the lack of a specific, sensitive indicator of zinc status. Presently, no good method for assessment of human zinc requirements exists.

• Preventive Nutrition and Food Science
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• v.2 no.3
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• pp.219-224
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• 1997

The pancreas is an important organ in the maintenance of zine homeostasis. The pancreatic tissue used in this study was obtained from rats fed varying levels of dietary Ca nd phytate followed by intraperitoneal {TEX}${65}^Zn${/TEX} injection. THe objective of this study was to determine the molecular size and distribution of compounds that may represent zinc-binding complexes in pancreatic tissue homogenates. The supernatant of the homogenized pancreatic tissue was separated using a Sephadex G-75 column with Tris buffer at pH 8.1. All subfractions were assayed for zinc, protein and {TEX}${65}^Zn${/TEX} activity. The elution of subfractions from pancreatic tissue homogenates showed a prominent peak corresponding to the high molecular weight protein standard (>66kd). A sall molecular weigth protein (<6.5kd), that was absorbed at 280nm, was also present: prominently in low Ca group, however not much as in high Ca group. These small compounds may combine weakly with zinc in pancreatic tissue an serve as zinc-binding ligands in pancreatic/biliary fluid. In the duodenum, these ligands dissociate zinc into an ionic form which becomes vulnerable to phytate complexation.

• Toxicological Research
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• v.23 no.1
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• pp.33-38
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• 2007

Zinc is an endogenous transition metal that can be synaptically released during neuronal activity. However, zinc may contribute to the neuropathology associated with a variety of conditions. Carnosine expressed in glial cells can modulate the effects of zinc on neuronal excitability as a zinc chelator. We hypothesize that carnosine may protect against neurotoxicity of zinc in cortical neuronal cells. The cortical neuronal cells from newborn rats were prepared and exposed to zinc chloride and/or carnosine at various concentrations. Zinc at the doses of 0 to $500{\mu}M$ decreased neuronal cell viability in a dose-dependent manner. Additionally, at the concentrations of 100 and $200{\mu}M$, it significantly decreased cell viability in an exposed time-dependent manner (p < 0.05). Treatment with carnosine at the concentrations of 20 and $200{\mu}M$ significantly increased neuronal cell proliferation by approximately 14% and 20%, respectively, compared to the control (p < 0.05). At the concentrations of 100 and $200{\mu}M$ zinc, $20{\mu}M$ carnosine significantly increased the viability of neuronal cells by 18.3% and 12.1 %, and $200{\mu}M$ carnosine also increased it by 33.5% and 28.6%, respectively, compared to the normal control group (p < 0.01). These results suggest that carnosine at a physiologically relevant level may protect against zinc-mediated toxicity in neuronal cells as an endogenous neuroprotective agent.

• Radiation Oncology Journal
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• v.33 no.2
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• pp.66-74
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• 2015

Trace elements play crucial role in the maintenance of genome stability in the cells. Many endogenous defense enzymes are containing trace elements such as superoxide dismutase and metalloproteins. These enzymes are contributing in the detoxification of reactive oxidative species (ROS) induced by ionizing radiation in the cells. Zinc, copper, manganese, and selenium are main trace elements that have protective roles against radiation-induced DNA damages. Trace elements in the free salt forms have protective effect against cell toxicity induced by oxidative stress, metal-complex are more active in the attenuation of ROS particularly through superoxide dismutase mimetic activity. Manganese-complexes in protection of normal cell against radiation without any protective effect on cancer cells are more interesting compounds in this topic. The aim of this paper to review the role of trace elements in protection cells against genotoxicity and side effects induced by ionizing radiation.

• BMB Reports
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• v.36 no.1
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• pp.128-137
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• 2003

Matrix metalloproteinases (MMPs), zinc dependent proteolytic enzymes, cleave extracellular matrix (ECM: collagen, laminin, firbronectin, etc) as well as non-matrix substrates (growth factors, cell surface receptors, etc). The deregulation of MMPs is involved in many diseases, such as tumor metastasis, rheumatoid arthritis, and periodontal disease. Metastasis is the major cause of death among cancer patients. In this review, we will focus on the roles of MMPs in tumor metastasis. The process of metastasis involves a cascade of linked, sequential steps that involve multiple host-tumor interactions. Specifically, MMPs are involved in many steps of tumor metastasis. These include tumor invasion, migration, host immune escape, extravasation, angiogenesis, and tumor growth. Therefore, without MMPs, the tumor cell cannot perform successful metastasis. The activities of MMPs are tightly regulated at the gene transcription levels, zymogen activation by proteolysis, and inhibition of active forms by endogenous inhibitors, tissue inhibitor of metalloproteinase (TIMP), and RECK. The detailed regulations of MMPs are described in this review.