• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.164.2-165
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• 2003

Chronic exposure of arsenic is well known to be the cause of cardiovascular disease such as hypertension. In order to investigate the effect of arsenic on blood vessels. we examined whether arsenic affected agonist-induced contraction of aortic rings in isolated organ bath system. Treatment with arsenite increased vasoconstriction induced by phenylephrine or serotonin in a concentration-dependent manner. (omitted)

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.1
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• pp.163.2-164
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• 2003

Several epidemiological 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 rings in vitro organ bath system.Treatment with arsenite inhibited acetylcholine-induced relaxation of aortic rings in a concentration-dependent manner. (omitted)

• 대한약학회:학술대회논문집
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• 대한약학회 2003년도 Proceedings of the Convention of the Pharmaceutical Society of Korea Vol.2-1
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• pp.71-71
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• 2003

Several epidemiological 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 rings in in vitro organ bath system. (omitted)

• Reproductive and Developmental Biology
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• 제38권3호
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• pp.107-114
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• 2014

Oral exposure of humans by excess amounts of arsenic may cause disturbances of the reproductive system. In the present study, such exposure was modelled in rats, with the support of sperm principal parameters and histopathological observations. Male Sprague-Dawley rats were randomly divided into three groups where the group I was served as a normal control, group II was received sodium meta-arsenite as arsenic (10 mg/kg b.w/day) and a combination of sodium meta-arsenite and sodium selenite (3 mg/kg b.w/day) in group III. After 6 weeks, there was no significant change in testis weight and in total motility of all the three experimental groups, whereas, rapid moving spermatozoa, moderately moving spermatozoa and slow moving spermatozoa were significantly decreased in arsenic treated rats as compared to control rats. The other sperm principal parameters like progressiveness, average path velocity, straightness linear velocity (VSL), curvilinear velocity (VCL), straightness, linearity sperm head elongation ratio, area, linearity amplitude of lateral head department (ALH) and beat cross frequency (BCF) were found to be reduced in arsenic intoxicated rats. These results are not correlated with the histological studies. On oral administration of selenium ameliorated the adverse effects of arsenic as compared to arsenic alone treated rats. Our findings clearly demonstrate that administration of selenium could prevent some of the deleterious effects of arsenic in the testis.

• 한국식품위생안전성학회:학술대회논문집
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• 한국식품위생안전성학회 2002년도 춘계학술발표대회 및 심포지움
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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.

• Fisheries and Aquatic Sciences
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• 제18권2호
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• pp.195-202
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• 2015

The effects of waterborne arsenic (As) exposure on bioaccumulation and antioxidant defenses were examined in the liver and gills of tilapia, Oreochromis niloticus, under thermal stress. Tilapia were exposed to different As concentrations (0, 200, and $400{\mu}g\;L^{-1}$) at three water temperatures (20, 25, and $30^{\circ}C$) for 20 days. After As exposure, higher levels of As accumulation were observed in the gills compared with the liver in elevated water temperatures. In terms of the antioxidant response, glutathione (GSH) levels and the activities of glutathione reductase (GR), glutathione peroxidase (GPx), and glutathione S-transferase (GST) significantly decreased in the liver and gills of tilapia exposed to As for 20 days, regardless of the As concentration (200 and $400{\mu}g\;L^{-1}$) or water temperature. These enzyme activities exhibited greater fluctuations in the liver and gills of tilapia after As exposure in water warmer than $20^{\circ}C$. The present findings suggest that the simultaneous stress of temperature change and As exposure can accelerate As accumulation and alter the antioxidant enzymes activities of tilapia.

• Asian-Australasian Journal of Animal Sciences
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• 제25권9호
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• pp.1262-1268
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• 2012

The present investigation was designed to determine whether supplementation of different level of vitamin E for 12 months to arsenic exposed goats (50 ppm as sodium arsenite) affords protection against the blood hemato-biochemical parameters caused by the metalloid. A total of 24 crossbred (Alpine${\times}$Beetal) lactating goats were assigned randomly into 4 equal groups (control, $T_1$, $T_2$ and $T_3$) of 6 in each, on the basis of average body weight ($36.10{\pm}0.11$ kg) and milk yield ($1.61{\pm}0.04$ kg/d). The animals in $T_1$, $T_2$ and $T_3$ were given 50 ppm arsenic, while in $T_2$ and $T_3$, additionally; vitamin E at the rate of 100 IU and 150 IU/kg dry matter (DM) respectively was additionally supplemented for the period of 12 months. Hemoglobin (Hb), total leukocyte (TLC) and blood lymphocyte % were decreased (p<0.05) in arsenic fed groups and vitamin E supplementation in the experimental group showed a protective potential. Significant increases (p<0.05) in aspertate transaminase (AST) and alanine transaminase (ALT) activities among arsenic supplemented groups were recorded, however vitamin E supplementation at higher doses showed a protective effect (p<0.05) against AST but in the case of ALT no ameliorating effect was found in either of the doses. Plasma total protein was decreased (p>0.05) but creatinine level was periodically increased in all As supplemented groups and vitamin E supplementation did not produce any protective effect. It can be concluded that arsenic exposure resulted in varying degree of changes in hemato-biochemical parameters and activities of antioxidant enzymes in goats but concomitant treatment with Vitamin E is partially helpful in reducing the burden of arsenic induced effect.

• Asian Pacific Journal of Cancer Prevention
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• 제13권6호
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• pp.2943-2948
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• 2012

Arsenic exposure is a serious health hazard worldwide. We have previously established that it may result in immune suppression by upregulating Th2 cytokines while downregulating Th1 cytokines and causing lymphocytic death. Treatment modalities for arsenic poisoning have mainly been restricted to the use of chelating agents in the past. Only recently have combination therapies using a chelating agent in conjunction with other compounds such as anti-oxidants, micronutrients and various plant products, been introduced. In the present study, we used T11TS, a novel immune potentiating glycopeptide alone and in combination with the sulfhydryl-containing chelator, mono-iso-amyl-dimarcaptosuccinic acid (MiADMSA) as a therapeutic regimen to combat arsenic toxicity in a mouse model. Results indicated that Th1 cytokines such as TNF-${\alpha}$, $IFN{\gamma}$, IL12 and the Th2 cytokines such as IL4, IL6, IL10 which were respectively downregulated and upregulated following arsenic induction were more efficiently restored to their near normal levels by T11TS alone in comparison with the combined regimen. Similar results were obtained with the apoptotic proteins studied, FasL, BAX, BCL2 and the caspases 3, 8 and 9, where again T11TS proved more potent than in combination with MiADMSA in preventing lymphocyte death. The results thus indicate that T11TS alone is more efficient in immune re-establishment after arsenic exposureas compared to combination therapy with T11TS+MiADMSA.

• Environmental Analysis Health and Toxicology
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• 제21권1호
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• pp.1-11
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• 2006

Arsenic is a ubiquitous element found in several forms in environment. Although certain foods, such as marine fish, contain substantial levels of organic arsenic forms, they are relatively low in toxicity compared to inorganic forms. In contrast, arsenic in drinking water is predominantly inorganic and very toxic. Chronic ingestion of arsenic-contaminated drinking water is therefore the major pathway posing potential risk to human health. World populations are exposed to low to moderate levels of arsenic of parts per billion (ppb) to thousands of ppb. When exposed to human, it could metabolize into monomethylarsonous acid ($MMA^{III}$) and dimethylarsinous acid ($DMA^{III}$) which are highly toxic. Lots of stuides have been recently focused how $MMA^{III}\;and\;DMA^{III}$ induce toxic insults in various target tissues. Epidemiological studies revealed that chronic arsenic exposure caused cancer, cardiovascular diseases, and diabetes etc. In this review, the current understanding of arsenic on health effects will be discussed.

• Toxicological Research
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• 제17권
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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.