• Title/Summary/Keyword: Calcium toxicity

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Effect of dietary Calcium Level on Cadmium and Lead Toxicity in Rats (식이내 Calcium 수준이 흰쥐의 카드뮴과 납중독에 미치는 영향)

  • 김미경
    • Journal of Nutrition and Health
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    • v.29 no.9
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    • pp.958-970
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    • 1996
  • This study was performed to investigate the effect of dietary calcium level on cadmium and lead toxicity in rats. Fifty-four male rats of Sprague-Dawely strain weighing 152$\pm$12g were blocked into 9 groups according to body weight, and were raised for 30 days. Nine experimental diets different with cadmium(0%, 0.04%), lead (0%, 0.071%) and calcijm(0.5%, 1.0%, 1.5%) levels were prepared. The results are summarized as follow. Weight gain, F.E.R.(food efficiency ratio), and weights of liver, kidney and femur were lower in cadmium exposed groups than those of heavy metal free groups. Weight gain F.E.R. and ash weight of lead groups were lower than those of heavy metal free groups. But, these were increased with increasing dietary calcium level. Cadmium and lead concentrations in blood, liver, kidney and femur were lower in rats fed 1.5% calcium than 0.5% calcium diet. Fecal cadmium and lead excretions were remarkably increased in 1.5% calcium groups, and cadmium and lead retention rates were decreased in 1.5% calcium groups. Metallothionein concentrations in liver, kidney and small intestine were higher in rats exposed to cadmium and lead. Calcium content in blood, femur and daily urinary and fecal calcium excretion were decreased by cadmium and lead additions, and increased in 1.5% calcium groups. Creatinine clearance were decreased with cadmium administratino and calcium addition. In conclusion, weight gain and organ weights were decreased with cadmium or lead administration. But, cadmium administration was more toxic than lead adminstration. Cadmium or lead toxicity was alleviated by increasing dietary calcium level. Especially, lead toxicity was alleviated in proportion to dietary calcium level.

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Antiarrhythmic effects of ginsenoside Rg2 on calcium chloride-induced arrhythmias without oral toxicity

  • Gou, Dongxia;Pei, Xuejing;Wang, Jiao;Wang, Yue;Hu, Chenxing;Song, Chengcheng;Cui, Sisi;Zhou, Yifa
    • Journal of Ginseng Research
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    • v.44 no.5
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    • pp.717-724
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    • 2020
  • Background: Malignant arrhythmias require drug therapy. However, most of the currently available antiarrhythmic drugs have significant side effects. Ginsenoside Rg2 exhibits excellent cardioprotective effects and appears to be a promising candidate for cardiovascular drug development. So far, the oral toxicity and antiarrhythmic effects of Rg2 have not been evaluated. Methods: Acute oral toxicity of Rg2 was assessed by the Limit Test method in mice. Subchronic oral toxicity was determined by repeated dose 28-day toxicity study in rats. Antiarrhythmic activities of Rg2 were evaluated in calcium chloride-induced arrhythmic rats. Antiarrhythmic mechanism of Rg2 was investigated in arrhythmic rats and H9c2 cardiomyocytes. Results: The results of toxicity studies indicated that Rg2 exhibited no single-dose (10 g/kg) acute oral toxicity. And 28-day repeated dose treatment with Rg2 (1.75, 3.5 and 5 g/kg/d) demonstrated minimal, if any, subchronic toxicity. Serum biochemical examination showed that total cholesterol in the high-dose cohort was dramatically decreased, whereas prothrombin time was increased at Day 28, suggesting that Rg2 might regulate lipid metabolism and have a potential anticoagulant effect. Moreover, pretreatment with Rg2 showed antiarrhythmic effects on the rat model of calcium chloride induced arrhythmia, in terms of the reduced duration time, mortality, and incidence of malignant arrhythmias. The antiarrhythmic mechanism of Rg2 might be the inhibition of calcium influx through L-type calcium channels by suppressing the phosphorylation of Ca2+/calmodulin-dependent protein kinase II. Conclusion: Our findings support the development of Rg2 as a promising antiarrhythmic drug with fewer side effects for clinical use.

Acute/Subacute Toxicity of Nano Calcium (나노 칼슘의 급성/아급성 안전성 평가)

  • Jung, Eun Young;Suh, Hyung Joo
    • Journal of the Korean Society of Food Science and Nutrition
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    • v.44 no.1
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    • pp.29-34
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    • 2015
  • The objective of this study was to obtain data on the safety-in-use of nano calcium as a dietary supplement by assessing its acute and subacute oral toxicities in female and male Sprague-Dawley rats. A single oral dose of 5,000 mg/kg of nano calcium did not result in mortality or significant changes in the general behavior and gross appearance of the internal organs of rats. For subacute toxicity study, nano calcium was administered orally at a dose of 1,000 mg/kg daily for 14 days. There were no significant differences in organ weights between control and treated groups of both sexes. Hematological analysis and blood chemistry revealed no toxic effects of nano calcium. Pathologically, neither gross abnormalities nor histopathological changes were observed. These results show that nano calcium possesses very low toxicity as indicated in a rat model.

Effect of zinc and calcium on the intracelularly uptake of cadimium and growth of escherichia coli

  • Hong, Hyo-Bong;Brown, Lewis R.;Kim, Jong-Kyu
    • Journal of Microbiology
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    • v.33 no.4
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    • pp.302-306
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    • 1995
  • E. coli was tested for their ability to uptake cadmium intracellularly, and the effect of zinc and calcium on cadmium toxicity to E. coli was observed. In addition, the effect of zinc and calcium on the uptake of cadimium was also studied. This study showed that living E. coli cells took up more cadmium than the dead cells. E. coli in the log phase uptake cadimiumm more actively than E. coli in the stationary phase. These results suggested that there may be metabolic reactions or compounds which encourage the uptake of cadimium. This study also showed that cadimium was sequestered by cell components of which molecular weight is about 30,000. Adding of zinc and calcium chloride reduced cadmium toxicity in E. coli and encouraged intracellular uptake by E coli. However adding of heavy metal solutions helped the microorganisms to adsorb more cadmium. Extremely high or low concentrations of zinc, however, did not affect cell viability.

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Quercetin ameliorates glutamate toxicity-induced neuronal cell death by controlling calcium-binding protein parvalbumin

  • Kang, Ju-Bin;Park, Dong-Ju;Shah, Murad-Ali;Koh, Phil-Ok
    • Journal of Veterinary Science
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    • v.23 no.2
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    • pp.26.1-26.12
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    • 2022
  • Background: Glutamate is the main excitatory neurotransmitter. Excessive glutamate causes excitatory toxicity and increases intracellular calcium, leading to neuronal death. Parvalbumin is a calcium-binding protein that regulates calcium homeostasis. Quercetin is a polyphenol found in plant and has neuroprotective effects against neurodegenerative diseases. Objectives: We investigated whether quercetin regulates apoptosis by modulating parvalbumin expression in glutamate induced neuronal damage. Methods: Glutamate was treated in hippocampal-derived cell line, and quercetin or vehicle was treated 1 h before glutamate exposure. Cells were collected for experimental procedure 24 h after glutamate treatment and intracellular calcium concentration and parvalbumin expression were examined. Parvalbumin small interfering RNA (siRNA) transfection was performed to detect the relation between parvalbumin and apoptosis. Results: Glutamate reduced cell viability and increased intracellular calcium concentration, while quercetin preserved calcium concentration and neuronal damage. Moreover, glutamate reduced parvalbumin expression and quercetin alleviated this reduction. Glutamate increased caspase-3 expression, and quercetin attenuated this increase in both parvalbumin siRNA transfected and non-transfected cells. The alleviative effect of quercetin was statistically significant in non-transfected cells. Moreover, glutamate decreased bcl-2 and increased bax expressions, while quercetin alleviated these changes. The alleviative effect of quercetin in bcl-2 family protein expression was more remarkable in non-transfected cells. Conclusions: These results demonstrate that parvalbumin contributes to the maintainace of intracellular calcium concentration and the prevention of apoptosis, and quercetin modulates parvalbumin expression in glutamate-exposed cells. Thus, these findings suggest that quercetin performs neuroprotective function against glutamate toxicity by regulating parvalbumin expression.

Reduction of Aluminum Toxicity by Calcium and Magnesium in Pines (소나무속 식물에서 칼슘과 마그네슘에 의한 알루미늄 독성의 경감)

  • Ryu, Hoon;Joon-Ho Kim
    • The Korean Journal of Ecology
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    • v.19 no.3
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    • pp.193-199
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    • 1996
  • Alleviation of Al toxicity by Ca and Mg was studied with seedings of Pinus densiflora, P. rigida and P. thunbergii under the solution culture. The seedlings were cultivated in the enriched Can and Mg nutrient solution with 2, 000 ${\mu}M$ Al for three weeks. The hightest total root lengths of P. densiflora, P. rigida and P. thunbergii increased by 21, 33 and 133% in Ca enriched solution, and 23, 44 and 107% in Mg enriched solution, respectively. Ratios of lateral root to main root length increased significantly in Mg enriched solution, and redution of Al toxicity was more affected by enriched Mg than by enriched Ca. Al content in tissue was reduced by enriched Ca and Mg.

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Cytotoxicity of Root Canal Sealers Containing Calcium Hydroxide

  • Kim, In-Geol;Han, Se-Hee;Cho, Young-Gon;Lee, Sang-Bae;Kim, Kwang-Mahn;Kim, Kyoung-Nam
    • Journal of Korean Dental Science
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    • v.2 no.1
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    • pp.11-18
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    • 2009
  • The purpose of this study was to investigate the possibility to reduce the toxicity of oil based root canal sealers containing calcium hydroxide using MTT & agar overlay assays. Thus some formulations of traditional root canal sealers were replaced with oil-soluble solvents and experimental root canal sealers manufactured. In MTT assay, Cell viability of all experimental sealers in addition with oil soluble solvents were observed significantly higher than both control groups, especially according to replace zinc and/or calcium ion components. Also agar overlay assay was appeared moderate to no cell responses into modifying both zinc and/or calcium ion components and oil soluble solvent weight. Authors found the reducing effect of cell toxicity through significant role of oil soluble solvent factor into root canal sealer containing calcium hydroxide.

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A STUDY ON THE CYTOTOXICITY OF THE ROOT CANAL SEALERS (근관충전용(根管充塡用) sealer의 세포독성(細胞毒性)에 관한 연구(硏究))

  • Lee, Seung-Jong;Kim, Yung-Hai
    • Restorative Dentistry and Endodontics
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    • v.16 no.1
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    • pp.25-40
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    • 1991
  • Four root canal sealers, Apatite Root Sealer I and II composed mainly of hydroxyapatite/tricalciumphosphate, Sealapex containing calcium hydroxide, and Roth Sealer composed of zinc oxide - eugenol were compared on the culture of L929 fibroblasts. MIT (Methyl Thiazole Tetrazolium Bromide) colorimetric technique was used to measure the mitochondrial dehydrogenase activity. Results were as follows: 1. Hydroxyapatite/tricalcium phosphate mixed sealers were significantly less toxic compared with calcium hydroxide and zinc oxide - eugenol type sealers. High pH of the calcium hydroxide sealer and release of eugenol component from the zinc oxide - eugenol type sealer were presumed to be the cause of the toxicity of these two sealers. In no cases, there were more cytoblastic effects in hydroxyapatite/tricalcium phosphate mixed sealers compared to the control groups. 2. In all experimental groups, toxicity was decreased as dilutions were increased. However in zinc oxide-eugenol type sealer the cell activity was weakened for all dilution groups. 3. Regarding the effect of setting time, Apatite I and Sealapex were less toxic as the setting progressed. Apatite II kept constant regardless of the different time ellapsed after setting but Roth sealer revealed significantly higher toxicity for all experimental groups. 4. Comparing two different culture periods of 24 hours and 72 hours, Apatite I showed higher cell activities in longer period(72 hours) while Apatite II did not. Sealapex and Roth sealer, however, showed significantly lower cell activities in longer period.

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Review on the mechanism for the reduction of raphide-induced toxicity via processing of Pinelliae Tuber and Arisaematis Rhizoma (포제(炮製)에 의한 반하(半夏)와 천남성(天南星)의 침상결정 유발 독성 감소 기전 고찰)

  • Kim, Jung-Hoon;Lee, Guemsan;Choi, Goya;Kim, Young-Sik;Lee, Seungho;Kim, Hongjun
    • The Korea Journal of Herbology
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    • v.36 no.5
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    • pp.15-27
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    • 2021
  • Objectives : The processing of Pinelliae Tuber and Arisaematis Rhizoma is a crucial step to reduce the severe acrid irritation mainly due to the needle-like crystals (raphides). Ginger, alum and bile juice have been used as adjuvant materials for the processing. Methods : Bibliographic research on ancient processing and experimental processing was performed to investigate the toxicity reduction mechanisms of the processing with ginger, alum and bile juice. Results : Ginger has been a major adjuvant for the processing of Pinelliae Tuber, followed by alum and bile juice since Song (宋) and Myeong (明) dynasties, and Arisaematis Rhizoma has been mainly used as Damnamseong (膽南星). The raphides consisting of calcium oxalate, lectin, agglutinin and polysaccharides can induce acrid irritation and the inflammatory reactions. The lipophilic components in the ginger denatured the structure of raphides and 6-gingerol-contained ginger extract attenuated the inflammatory reaction. The calcium ion (Ca2+) of calcium oxalate was substituted to the aluminium ion (Al3+) of the alum, which damaged the calcium oxalate structure. Lectin attached to the surface of raphides was dissolved in alum solution and consequently its structure was denatured. The cholate in the bile juice formed the complex with the oxalate anion or the calcium cation. Moreover, the enzymes activated by Lactobacillus or Bifidobacterium during the fermentation promoted the fragmentation of oxalate. Conclusion : The adjuvant materials damaged the raphides by denaturing or degrading the calcium oxalate, resulting in the reduction of acrid irritation. Further experimental studies would support the toxicity reduction mechanism of the processing.

The underlying mechanism of calcium toxicity-induced autophagic cell death and lysosomal degradation in early stage of cerebral ischemia

  • Jirakhamon Sengking;Pasuk Mahakkanukrauh
    • Anatomy and Cell Biology
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    • v.57 no.2
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    • pp.155-162
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    • 2024
  • Cerebral ischemia is the important cause of worldwide disability and mortality, that is one of the obstruction of blood vessels supplying to the brain. In early stage, glutamate excitotoxicity and high level of intracellular calcium (Ca2+) are the major processes which can promote many downstream signaling involving in neuronal death and brain tissue damaging. Moreover, autophagy, the reusing of damaged cell organelles, is affected in early ischemia. Under ischemic conditions, autophagy plays an important role to maintain energy of the brain and its function. In the other hand, over intracellular Ca2+ accumulation triggers excessive autophagic process and lysosomal degradation leading to autophagic process impairment which finally induce neuronal death. This article reviews the association between intracellular Ca2+ and autophagic process in acute stage of ischemic stroke.