• Journal of Nutrition and Health
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• v.53 no.4
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• pp.347-355
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• 2020

Purpose: Zinc is known to be associated with osteoblast proliferation and differentiation. Osterix as zinc-finger transcription factor is also related to osteoblast differentiation and bone formation. In the present study, we aimed to investigate whether zinc modulates osterix gene and protein expression in osteoblastic MC3T3-E1 cells. Methods: MC3T3-E1 cells were cultured in zinc-dependent concentrations (0, 0.5, 1, 5, or 15 µM Zn), along with osteogenic control (normal osteogenic medium) for 1 and 3 days. The gene and protein expression levels of osterix were analyzed by real-time reverse transcription polymerase chain reaction and Western blotting, respectively. Results: Zinc increased osteoblast proliferation in a concentration-dependent manner at day 1 and 3. Similarly, zinc increased the activity of osteoblast marker enzyme alkaline phosphatase in cells and media in a zinc concentration-dependent manner. Moreover, our results showed that the pattern of osterix gene expression by zinc was down-regulated within the low levels of zinc treatments (0.5-1 µM) at day 1, but it was up-regulated after extended culture period at day 3. Osterix protein expression by zinc showed the similar pattern of gene expression, which down-regulated by low zinc levels at day 1 and up-regulated back at day 3 as the early stage of osteoblast differentiation. Conclusion: Our results suggest that zinc modulates osterix gene and protein expression in osteoblasts, particularly in low level of zinc at early stage of osteoblast differentiation period.

• Journal of the Korean Society of Food Science and Nutrition
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• v.25 no.4
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• pp.601-607
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• 1996

Nineteen non-insulin-dependent diabetic(NIDD) and healthy control women were investigated to study the relationship between glycemic control and the level of calcium, zinc, and magnesium in the serum and urine. Urinary calcium, zinc and magnesium levels in the NIDD women were significantly higher(p<0.01) than those of the control women. There were no difference in serum magnesium and zinc levels between the two groups, but se겨m calcium level was lower(p<0.01) in the NIDD women compared to that of the control group. In the NIDD women, serum magnesium was negatively related to fasting blood glucose(r=-0.533 : p<0.05), urinary glucose(r=-0.767 ; P<0.001), urinary protein(r=-0.476 : p<0.05), and urine volume(r=-0.571 : p<0.05). The levels of zinc in both serum (r=0.515, p<0.05) and urine(r=0.623 : p<0.01) were related to urinary protein but only urinary zinc level(r=0.570 : p<0.01) was related to serum albumin. Urinary magnesium, not calcium was correlated with the urinary glucose(r=0.563 : p<0.05) and urinary protein(r=0.568 ; p<0.05). Fasting blood glucose was positively correlated with duration of diabetes, as well as dietary fat and calorie intake. The results of this study suggest that NIDD alters all magnesium, zinc, and calcium utilization, particularly magnesium is involved in glycemic control in this condition.

• Nutritional Sciences
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• v.8 no.4
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• pp.242-249
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• 2005

It is well established that zinc plays an important role in bone metabolism and mineralization. The role of zinc in bone formation is well documented in animal models, but not much reported in cell models. In the present study, we evaluated zinc deficiency effects on osteoblastic cell proliferation, alkaline phosphatase activity and expression, and extracellular matrix bone nodule formation and bone-related gene expression in osteoblastic MC3T3-E1 cells. To deplete cellular zinc, chelexed-FBS and interpermeable zinc chelator TPEN were used. MC3T3-E1 cells were cultured in zinc concentration-dependent (0-15 ${\mu}M\;ZnCl_2$) and time-dependent (0-20 days) manners. MC3T3-E1 cell proliferation by MTT assay was increased as medium zinc level increased (p<0.05). Cellular Ca level and alkaline phosphatase activity were increased as medium zinc level increased (p<0.05). Alkaline phosphatase expression, a marker of commitment to the osteoblast lineage, measured by alkaline phosphatase staining was increased as medium zinc level increased. Extracellular calcium deposits measured by von Kossa staining for nodule formation also appeared higher in Zn+(15 ${\mu}M\;ZnCl_2$) than in Zn-(0 ${\mu}M\;ZnCl_2$). Bone formation marker genes, alkaline phosphatase and osteocalcin, were also expressed higher in Zn+ than in Zn-. The current work supports the beneficial effect of zinc on bone mineralization and bone-related gene expression. The results also promote further study as to the molecular mechanism of zinc deficiency for bone formation and thus facilitate to design preventive strategies for zinc-deficient bone diseases.

• Nutrition Research and Practice
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• v.4 no.5
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• pp.356-361
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• 2010

Zinc is an essential trace element required for bone formation, however not much has been clarified yet for its role in osteoblast. We hypothesized that zinc would increase osteogenetic function in osteoblasts. To test this, we investigated whether zinc treatment enhances bone formation by stimulating osteoblast proliferation, bone marker protein alkaline phosphatase activity and collagen synthesis in osteoblastic MC3T3-E1 cells. MC3T3-E1 cells were cultured and treated with various concentrations of zinc (0, 1, 3, 15, 25 uM) along with a normal osteogenic medium (OSM) as control for 1, 5, 10 days. As measured by MTT assay for mitochondrial metabolic activity, cell proliferation was stimulated even at low zinc treatment (1-3 ${\mu}M$) compared to OSM, and it was stimulated in a zinc concentration-dependent manner during 5 and 10 days, with the most pronounced effect at 15 and 25 uM Zn. Cellular (synthesized) alkaline phosphatase (ALP) activity was increased in a zinc concentration-dependent manner, so did medium (secreted) ALP activity. Cellular collagen concentration was increased by zinc as time went by, therefore with the maximum zinc stimulatory effect in 10 days, and medium collagen concentration showed the same pattern even on 1 and 5 day. This zinc stimulatory effect of collagen synthesis was observed in cell matrix collagen staining. The study results imply that zinc can increase osteogenic effect by stimulating cell proliferation, ALP activity and collagen synthesis in osteoblastic cells.

• Journal of Sericultural and Entomological Science
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• v.45 no.2
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• pp.121-125
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• 2003

Dissolution of Antheraea pernyi silk fiber was carried out in a zinc nitrate 6 hydrate (Zn(NO$_3$)$_2$ㆍ6$H_2O$) solution with various dissolving conditions. The solubility was significantly dependent on the concentration of zinc nitrate, dissolving temperature and time. Regenerated A. pernyi silk fibroin powder was obtained through dialysis process to remove chaotropic salt. FTIR and X-ray diffractometer showed that the conformation of regenerated A. pernyi silk powder was sheet structure.

• Asian-Australasian Journal of Animal Sciences
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• v.18 no.3
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• pp.439-452
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• 2005

Zinc is ubiquitous in all living cells. Structural and catalytic properties of cellular enzymes are zinc dependent. Zinc deficiency leads to a variety of pathological abnormalities with immune impairment. It is an established fact that nutritional status contributes to overall immune response of individuals. Outcome of zinc deficiency on immune system is so drastic that it is difficult to conceive at the first instance. Zinc supplementation has been advocated to prevent diarrheal disease in children with poor nutritional status. The bioavailability of zinc depends upon its sources. Moreover it varies between monogastrics and ruminants. Controversy still prevails between inorganic and organic sources of zinc with respect to their superiority in bioavailability. Zinc exerts immunostimulatory effects in various laboratory and farm animals. Animals having congenital zinc deficiency diseases like A46 lethal trait usually die due to impairment of the immune system unless treated with zinc. The immune mechanism of zinc and its effect on animals and man are discussed. Zinc has been considered as extremely safe at higher therapeutic doses, but does not provide any beneficial effect but rather may cause immunosuppression. More recently, zinc has been prescribed for immunodeficient hosts, to modulate the immune system so that to a certain extent it can combat against opportunistic pathogens.

• Environmental Analysis Health and Toxicology
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• v.19 no.4
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• pp.389-399
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• 2004

Metallothionein (MT), a small protein molecule which can bind or release metal ions, is involved in the regulation of cellular metal homeostasis. This study was investigated the accumulation of cadmium in blood, tissue (liver, kidney and brain), and the effect of cadmium on several key genes (MT-I, MT-II, ZnT-1) in zinc metabolism in the mouse. Mouses weighing 20∼25 g were randomly assigned to control and cadmium treated group (Cd group). Cd group was intraperitoneally injected with cadmium 2, 4, 8 mg/kg and control group was administerd with saline. Mouses of each group were sacrificed by decapitation 4 hours after the administration of cadmium. Cadmium contents in blood, liver, kidney and brain were increased by a dose-dependent manner. Accumulation of cadmium was mainly occurred in liver and kidney. Induction of MT-I and MT-II protein was increased, but ZnT-1 expression was decreased in a dose-dependent manner by the treatment of 2∼8 mg/kg cadmium. These results suggested that cadmium can be transported to brain and alter the expression of several key genes in zinc homeostasis.

• Toxicological Research
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• v.16 no.3
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• pp.179-185
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• 2000

Zinc is known to generate reactive oxygen species (ROS) including superoxide anion and hydrogen peroxide ($H_2O_2$), which eventually contribute to cytotoxicity in a variety of cell types. Here in, we demonstrated that zinc decreased the viability of C6 glial cells in a time and dose-dependent manner, which was revealed as apoptosis characterized by ladder-pattern fragmentation of genomic DNA. chromatin condensation and DNA fragmentation in Hoechst dye staining. Zinc-induced apoptosis of C6 glial cells was prevented by the addition of catalase and antioxidants including reduced glutathione (GSH), N-acetyl-L-cysteine (NAC) and pyrrolidinedithiocarbamate (PDTC). Wefurther confirmed that zinc decreased intrac-ellular levels of GSH and generated $H_2O_2$in C6 glial cells. Moreover, antioxidants also decreased the generation of zinc-induced $H_2O_2$ in C6 glial cells. These data indicated that zinc-induced the apoptotic death of C6 glial cells via generation of reactive oxygen species such as $H_2O_2$.

• Journal of the Korean Magnetic Resonance Society
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• v.22 no.4
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• pp.144-148
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• 2018

Catalytic enzyme Pyrazinamidase (PncA) from Mycobacterium tuberculosis can hydrolyze substrate pyrazinamide (PZA) to pyrazoic acid (POA) as active form of compound. Using NMR spectroscopy, pH-dependent catalytic properties were monitored including metal binding mode during converting PZA to POA. There seems to be a conformational change through zinc binding in active site from the perturbation of peak intensities in series of 2D HSQC spectra the conformation changes through zinc binding.

• The Journal of Internal Korean Medicine
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• v.26 no.2
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• pp.409-419
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• 2005

The water extract of Boyanghwanoh-tang has been used for treatment of ischemic vascular disease in oriental medicine. However, little is known about the mechanism by which the water extract of Boyanghwanoh-tang rescues cells from these damages. Therefore, this study was designed to evaluate the protective effects of Boyanghwanoh-tang on zinc-mediated cytotoxicity in H9c2 cardiomyoblast cells. This study demonstrates that, after treatment of H9c2 cells with zinc, there was a decrease in cell viability in a dose dependent manner, and there was a chromatin condensation. Zinc induced the change of cell morphology. In addition, zinc induced mitochondrial dysfunction. Zinc-induced H9c2 cell death was remarkably prevented by the pretreatment of Boyanghwanoh-tang consistently with increase of the peroxoredoxin 1, 2, 3, 5, and 6 expression. Taken together, the results suggest that zinc induced severe cell death in H9c2 cardiomyoblast cells, and that protective effects of Boyanghwanoh-tang against oxidative injuries are achieved through regulation of peroxiredoin expression.