• Toxicological Research
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• v.16 no.4
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• pp.255-261
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• 2000

To investigate what kinds effect arsenic exert on the proliferation and differentiation of bone marrow cells to the neutrophilic granulocytes lineage cells, we treated sodium arsenite to murine bone marrow cells without or with the stimulation of G-CSF. When we added the various concentrations oj sodium arsenite to bone marrow cells without the stimulation of G-CSF for I, 3, 5 or 7 days, sodium arsenite did not make an any effect up to 2.5 $\mu\textrm{M}$$\mu\textrm{M}$$\mu\textrm{M}$$\mu\textrm{M}$$\mu\textrm{M}$$m\ell$ of G-CSF was induced by the co treatment of 12.5 $\mu\textrm{M}$

• The Korean Journal of Zoology
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• v.30 no.2
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• pp.99-106
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• 1987

It is the purpose to investigate the physiological toxity and mutagenicity by heavy metal compounds such as potasium dichromate, sodium arsenite and selenium dioxide on the development of Drosophila melanogaster. These chemical compounds were highly toxic at every developmental stage of Drosophila. The relative values of fecundity, viability and developmental time obtained on food media containing 5 different levels of potasium dichromate (500, 600, 700, 800, and 900 ppm), also 5 different levels of sodium arsenite and selenium dioxide (10, 15, 20, 25 and 30 ppm). Resulting in the relative values of fecundity and viability generally decreased, on the contrary developmental time generally reduced as the concentration of chemicals in the food increased. A significant reduction in the fecundity was observed between 800 and 900 ppm (p<0. 01) on the potasium dichromate media, between 15 and 20 ppm (p<0. 05) on the sodium arsenite media, between 20 and 25 ppm (p<0. 02) on the selenium dioxide media. A significant reduction in the viability was observed between 700 and 800 ppm (p<0. 01) on the potasium dioxide media, between 25 and 30 ppm (p<0. 01) on the sodium arsenite media, between 20 and 25 ppm (p<0. 01) on the selenium dioxide media. The developmental time was significantly reduced between 800 and 900 ppm (p<0. 001) on the potasium dioxide media, between 15 and 20 ppm (p<0. 001) on the sodium arsenite media, and between 25 and 30 ppm (p<0. 01) on the selenium dioxide media.

• The Korean Journal of Zoology
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• v.30 no.2
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• pp.107-116
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• 1987

It is the purpose to investigate the physiological toxity and mutagenicity by heavy metal compounds such as potasium dichromate, sodium arsenite and selenium dioxide on the development of Drosophila melanogaster. These chemical compounds were highly toxic at every developmental stage of Drosophila. The relative values of fecundity, viability and developmental time obtained on food media containing 5 different levels of potasium dichromate (500, 600, 700, 800, and 900 ppm), also 5 different levels of sodium arsenite and selenium dioxide (10, 15, 20, 25 and 30 ppm). Resulting in the relative values of fecundity and viability generally decreased, on the contrary developmental time generally reduced as the concentration of chemicals in the food increased. A significant reduction in the fecundity was observed between 800 and 900 ppm (p<0. 01) on the potasium dichromate media, between 15 and 20 ppm (p<0. 05) on the sodium arsenite media, between 20 and 25 ppm (p<0. 02) on the selenium dioxide media. A significant reduction in the viability was observed between 700 and 800 ppm (p<0. 01) on the potasium dioxide media, between 25 and 30 ppm (p<0. 01) on the sodium arsenite media, between 20 and 25 ppm (p<0. 01) on the selenium dioxide media. The developmental time was significantly reduced between 800 and 900 ppm (p<0. 001) on the potasium dioxide media, between 15 and 20 ppm (p<0. 001) on the sodium arsenite media, and between 25 and 30 ppm (p<0. 01) on the selenium dioxide media.

• Korean Journal of Plant Resources
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• v.27 no.4
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• pp.344-353
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• 2014

This study was carried out to analyze the effect of arsenic types on growth and arsenic accumulation ability of Pteris multifida. Among arsenic pollution sources, Sodium arsenate, Calcium arsenate, Sodium arsenite and Potassium arsenite were treated in horticultural compost contaminated with $500mg{\cdot}kg^{-1}$. P. multifida was cultivated for 12 weeks. The results of study, Calcium arsenate treatment showed slightly decreased growth of P. multifida. But, growth of P. multifida cultivated in the remaining arsenic treatment was similar to untreated control plot. With only short-term cultivation of 4 weeks, aerial part of P. multifida in Sodium arsenate treatment showed high arsenic accumulation of $2,289.5mg{\cdot}kg^{-1}DW$. The arsenic accumulation ($2,956.0mg{\cdot}kg^{-1}DW$) was the highest at 12 week. On the other hand, underground part showed the highest arsenic accumulation in Potassium arsenite treatment ($2,470.2mg{\cdot}kg^{-1}DW$) and Calcium arsenate treatment accumulated $1,060.7mg{\cdot}kg^{-1}DW$ of arsenic. Regardless of arsenic types, aerial part of P. multifida was absorbed more than $1000mg{\cdot}kg^{-1}DW$ of arsenic. And removal of arsenic in soil was also higher. Therefore, Pteris multida is considered to be suitable phytoremediation meterial of various arsenic contaminated areas.

• Toxicological Research
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• v.17
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• pp.59-69
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• 2001

Arsenic exposure is associated with several human diseases, including cancers, atherosclerosis, hypertension, and cerebrovascular diseases. In cultured cells, arsenite, an inorganic arsenic com-pound, was demonstrated to interfere with many physiological functions, such as enhancement of oxidative stress, delay of cell cycle progression, and induction of structural and numerical changes of chromosomes. The objective of this study is to investigate the effects of arsenic exposure on gene expression profiles by colorimetric cDNA microarray technique. HFW (normal human diploid skin fibroblasts), CL3 (human lung adenocarcinoma cell line), and HaCaT (immortalized human keratinocyte cell line) were treated with 5 $\mu\textrm{M}$ or 10 $\mu\textrm{M}$ sodium arsenite for 6 or 16 h, respectively. By a dual-color detection system, the expression profile of arsenite-treated cultures was compared to that of control cultures. Several genes expressed differentially were identified on the microarray membranes. For example, MDM2, SWI/SNF, ubiquitin specific protease 4, MAP3K11, RecQ protein-like 5, and Ribosomal protein Ll0a were consistently induced in all three cell types by arsenite, whereas prohibitin, cyclin D1, nucleolar protein 1, PCNA, Nm23, and immediate early protein (ETR101) were apparently inhibited. The present results suggest that arsenite insults altered the expression of several genes participating in cellular responses to DNA damage, stress, transcription, and cell cycle arrest.

• CELLMED
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• v.4 no.3
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• pp.20.1-20.7
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• 2014

Ethanolic leaf extract of Bauhinia variegata has been tested for its possible antioxidant potentials against sodium arsenite induced toxicity in mice. Mice were randomized into two groups of five and fifty mice. Group I consisting of 5 mice without any treatment with food and water ad libitum which served as normal control. Group II mice were fed with sodium arsenite in drinking water at 100 ppm concentration for two monthsthen they were segregated into five groups which were treated differently. Group II a mice received only arsenic as sodium arsenite with drinking water, Group II b were fed chronically 1 : 20 alcohol to distilled water (vehicle), Group II c, d, e mice were orally fed 50 mg/kg, 150 mg/kg and 250 mg/kg of B. variegata leaf extract of once daily for 15 and 30 days respectively along with arsenic. Several toxicity marker enzymes such as gamma glutamyl transferase, lactate dehydrogenase, aspartate and alanine aminotransferase, acid and alkaline phosphatase, catalase and superoxide dismutase along with haematological variables such as glucose 6-phosphate dehydrogenase, creatinine, bilirubin, haemoglobin and sugar in different groups of treated and control mice were studied. Results obtained from the in vivo experiment revealed that administration of sodium arsenite caused a significant increase in some enzymes while decrease in some. A similar trend was also observed with haematological variables. In contrast B. variegata treatment at 150 mg/kg favourably modulated these alterations and maintained the antioxidant status than other two doses i.e. 50 mg/kg and 250 mg/kg thereby making it a good candidate to be used as supportive palliating measures in arsenic induced toxicity.

• Applied Microscopy
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• v.24 no.4
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• pp.78-85
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• 1994

Sodium arsenite ($NaAsO_2$) was injected to the rat subcutaneously for the study of the acute toxicity of arsenite on hepatocytes, and the effects of pretreatment of arsenite and glutathione on the lethalty of the arsenite treated rats. Arsenite treated rat hepatocytes showed vacuolated cytosol and shrinked nuclear and expanded perinuclear space and cytoplasmic membrane whirl. Rats pretreated with BSO (L-Buthionine-SR-Sulfoximine), less survived than arsenite treated alone. It means that glutathione acts as a protecting agent against the arsenite. Subcutaneous sublethal dose (10mg/kg body weight) treatment was showed the protecting activity to lethality of lethal dose (15mg/kg body weight) treated rat. 10mg/kg body weight sublethal dose effects appeared in six hours intervals of between treatments.

• Proceedings of the Korean Society of Food Hygiene and Safety Conference
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• 2002.05a
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• pp.137-137
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• 2002

Several epidemiologidal studies suggested that arsenic exposure was strongly correlated with the development of cardiovascular disease such as hypertension. In order to examine whether arsenic affects vasomotor tone in blood vessels, we investigated the effect of arsenic on agonist-induced vasorelaxation using the isolated rat aortic ring in in vitro organ bath system. Treatment with arsenite inhibited acetylcholine-induced relaxation of aortic rings in a concentration- dependent manner. The inhibitory effects by arsenic were also observed in the relaxation induced by sodium nitroprusside, a NO-donor. Consistent with these findings, the cGMP levels stimulated by acetylcholine in blood vessels were reduced significantly by arsenite treatment. In addition, higher concentration of arsenite decreased the relaxation by 8-Br-cGMP, a cGMP analog, in aortic rings without endothelium. These in vitro results indicated that arsenite that arsenite was capable of suppressing acetylcholine-induced relaxation in blood vessels by inhibiting production of nitric oxide in endothelial cells and by impairing the relaxation machinary in smooth muscle cells. In vivo studies revealed that the reduction of blood pressure by acetylcholine infusion was signigicantly suppressed after arsenite was administered intravenously to rate. These data suggest that vasomotor tone impaired by arsenite exposure may be one of the contrbuting factors in development of cardiovascular disease.

• Journal of Microbiology and Biotechnology
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• v.17 no.5
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• pp.812-821
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• 2007

The ecosystems of certain abandoned mines contain arsenic-resistant bacteria capable of performing detoxification when an ars gene is present in the bacterial genome. The ars gene has already been isolated from Pseudomonas putida and identified as a member of the membrane transport regulatory deoxyribonucleic acid family. The arsenite-oxidizing bacterial strains isolated in the present study were found to grow in the presence of 66.7 mM sodium arsenate($V;\;Na_2HAsO_4{\cdot}7H_2O$), yet experienced inhibited growth when the sodium arsenite($III;\;NaAsO_2$) concentration was higher than 26 mM. Batch experiment results showed that Pseudomonas putida strain OS-5 completely oxidized 1 mM of As(III) to As(V) within 35 h. An arsB gene encoding a membrane transport regulatory protein was observed in arsenite-oxidizing Pseudomonas putida strain OS-5, whereas arsB, arsH, and arrA were detected in strain OS-19, arsD and arsB were isolated from strain RW-18, and arsR, arsD, and arsB were found in E. coli strain OS-80. The leader gene of arsR, -arsD, was observed in a weak acid position. Thus, for bacteria exposed to weak acidity, the ars system may cause changes to the ecosystems of As-contaminated mines. Accordingly, the present results suggest that arsR, arsD, arsAB, arsA, arsB, arsC, arsH, arrA, arrB, aoxA, aoxB, aoxC, aoxD, aroA, and aroB may be useful for arsenite-oxidizing bacteria in abandoned arsenic-contaminated mines.

• Environmental Mutagens and Carcinogens
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• v.26 no.2
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• pp.35-40
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• 2006

Background: Inorganic arsenic is a human carcinogen that can target the liver, but its carcinogenic mechanisms are still unknown. Inorganic arsenic induces a spectrum of tumors including hepatocellular carcinoma in mice. Methods: Pregnant C3H mice were supplied with drinking water containing 50 ppm sodium arsenite during their pregnancy. The protein expression profile in the liver of 0.5-day-old. male offsprings exposed transplacentally to sodium arsenite was analyzed using protein 2D gel electrophoresis followed by mass spectrometry (MALDI-TOF). Results: Expression of proteins such as hydroxymethylglutaryl-CoA synthase mitochondrial precursor (HMG-CoA synthase), ${\beta}$-actin (cytoplasmic 1) and apolipoprotein A-IV precursor (Apo-AIV) were induced in mouse liver by sodium arsenite, while uricase (urate oxidase), guanine nucleotidebinding protein beta subunit 2-like 1 (RACK1) and fructose-bisphosphate aldolase B (Aldolase 2) were down-regulated. Summary: Expression of proteins that have been implicated in carcinogenesis, such as HMG-CoA, ${\beta}$-actin, and RACK1, was regulated in the liver of mice transplacentally exposed to inorganic arsenic.