• Asian Pacific Journal of Cancer Prevention
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• v.16 no.15
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• pp.6397-6400
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• 2015

Cervical cancer is the second most common gynecological malignancy worldwide. According to HPV Information Centre, Spain (Aug'2014), in India approximately 1,22,844 women are diagnosed with the disease every year and of them 67,477 die due to the disease. CaCx is said to be mediated by HPV but recent data published reveal the role of Oxidative Stress in different Cancers. Arsenic is also one of the agents for causing Oxidative Stress. Arsenic has been linked with different types of cancer. Arsenic is considered responsible for generation of free radicals and eventually for apoptosis. Early diagnosis of CaCx is presently a matter of concern and clinical presentation in advanced stages become difficult for complete clinical response. For determination of oxidative stress, Malondialdehyde (MDA) was taken as an identifier and arsenic estimation was performed with the help of Atomic Absorption Spectrometer (AAS). RBC count and Haemoglobin levels were performed according to standard protocol. MDA was in direct proportion with arsenic concentration and inversely proportional to RBC and Haemoglobin in CaCx patients. Arsenic is one of the major causative agents for oxidative stress and hence may be a risk factor leading to cancer including CaCx.

• Korean Journal of Soil Science and Fertilizer
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• v.47 no.3
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• pp.213-216
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• 2014

Arsenic is a known hazardous metalloid not only to the animals but also to plants. With high concentrations, it can impede normal plant growth and cause even death of plants at extremely high levels. A known plant response to stress conditions such as toxic levels of metal (loids) is the production of stress ethylene, causing inhibitory effect on root growth in plants. When the effect of various arsenic concentrations was tested to maize plant, the stress ethylene emission proportionately increased with increasing concentration of As(V). The inoculation of two arsenic tolerant bacteria; Pseudomonas grimonti JS126 and Pseudomonas taiwanensis JS238 having respective high and low 1-aminocyclopropane-1-carboxylate (ACC) deaminase activity reduced stress ethylene emission by 59% and 30% in maize grown in arsenic polluted soils. The result suggested the possible use of Pseudomonas grimonti JS126 for phytoremediation of arsenic polluted soils.

• Environmental Analysis Health and Toxicology
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• v.21 no.1 s.52
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• pp.71-79
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• 2006

Epidemiologic studies have showed a close correlation between arsenic exposure and heart disease such as, cardiovascular problem, ischemic heart disease, infarction, atherosclerosis and hypertension in human. It may increase the mortality of high risk group with heart disease. Regarding the mechanism studies of heart failure, blood vessel, vascular smooth muscle cells and endothelial cells have long been focused as the primary targets in arsenic exposure but there are only a few studies on the cardiomyocytes. In this study, the generation of oxidative stress by low dose of arsenic trioxide was investigated in rat cardiomyocytes. By direct measurement of reactive oxygen species and fluorescent microscopic observation using fluorescent dye 2',7'-dichlorofluorescin diacetate, reactive oxygen species were found to be generated without cell death, where cells are treated with 0.1 ppm arsenic for 24 hours. With the induction of reactive oxygen species, GSH level was decreased by the same treatment. However, DNA damage did not seem to be serious by DAPI staining, while high dose of arsenic (2 ppm for 24 hrs) caused fragmentation of DNA. To identify the molecular biomarkers of low-dose arsenic exposure, gene expression was also investigated with whole genome microarray. As results, 9,022 genes were up-regulated including heme oxygenase-l and glutathione S-transrerase, which are well-known biomarkers of oxidative stress. 9,404 genes were down-regulated including endothelial type gp 91-phox gene by the treatment of 0.1 ppm arsenic for 24 hours. This means that biological responses of cardiomyocytes may be altered by ROS induced by low level arsenic without cell death, and this alteration may be detected clearly by molecular biomarkers such as heme oxygenase-1.

• Journal of Environmental Science International
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• v.12 no.6
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• pp.651-657
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• 2003

In order to examine if arsenic, one of environmental stresses, contributes to hypertension as one of cardiovas cular pathological factors, this study was perfarmed in vivo and in vitro, using intacted or pithed rats and aorta ring preparation, respectively. And also the relationship between expression of heat shock protein (HSP) 90 and vasoactives-induced contractile response was elucidated. To measure blood pressure, the carotid arterial pressure was recorded on physiograph(Grass Co. 79E) connected to strain gauge. On the other hand, contractile response of vascular ring preparation isolated from rat was determined in organ bath and was recorded on physiograph connected to isometric transducer. And HSP was detacted by Western blotting whole cell Iysis. Preganglionic nerve stimulation was increased by 26.0% in arterial pressure of rat treated with arsenic. Vascular contractile response was monitored and HSP were measured by Western blotting of whole Iysis prepared from samples exposed with 0, 0.5, 1, 2 and 4 mM of arsenic for 8 hours. The dose-vascular responses of potassium chloride were augmented by increasing dose of arsenic in the strips exposed to arsenic for 8 hours, and were not augmented for 1, 3, 5 hours. And the response of relaxation of rat aorta induced by histamine was not influenced by arsenic stress. The increase of HSP 90 expression in rat aorta was pronounced at 8 hours after 4 mM of arsenic treatment, but HSP 60 expression was not. Arsenic stress not only increased the expression of HSP 90 in the rat aorta, but also augmented contractions to potassium chloride. These results indicated that arsenic stress was sufficient to induce heat shock protein 90, resulting in increased vascular contractility in rat aorta.

• Journal of Life Science
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• v.13 no.5
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• pp.634-641
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• 2003

In order to examine whether arsenic, one of environmental stress, contribute to augumentation and relaxation of rat aorta, this study was performed in vivo and in vitro, using intacted or denuded rats aorta ring preparation, respectively. The carotid arterial pressure was recorded on an ink-writing physiograph(Grass Co. 79E) connected to strain gauge. The contractile response of vascular ring with or without endothelium preparation isolated from rat were determined in organ bath and was recorded on physiograph connected to isometric transducer. Vasopressin-,and phenylephrine- induced increase in arterial pressure significantly enhanced in arsenic-treated rats; increase of 19.1%, and 46.6%, respectively. Vascular contractile response was measured in vitro preparations exposed to 0, 0.5, 1, 2 and 4 mM of arsenic for 1, 3, 5 and 8 hours. The dose-vascular responses of phenylephrine augmented by increasing dose of arsenic in the strips exposed to arsenic for 8 hours, and did not augmented for 1, 3, 5 hours. The phenomenon was not affected by strips denuded endothelium. And the response of relaxation of rat aorta induced by nitroprusside was not influenced by arsenic stress, but acetylcholine was a little increased. compared to that of control. There were no significant difference in relaxation between control and arsenic treated rings with endothelium or denuded. All of the results, phenyleprine-induced vascular contraction was significantly enhanced in 4 mM arsenic-treated rat aortic rings compared with control, whether endothelium was present or denuded at 8 hours after arsenic treatment. It may be a mechanism by which long-term arsenic stresses play a role in development of hypertension.

• Asian Pacific Journal of Cancer Prevention
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• v.17 no.9
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• pp.4185-4197
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• 2016

Chronic arsenicosis is a major environmental health hazard throughout the world, including India. Animals and human beings are affected due to drinking of arsenic contaminated ground water, due to natural mineral deposits, arsenical pesticides or improperly disposed arsenical chemicals. Arsenic causes cancer with production of free radicals and reactive oxygen species (ROS) that are neutralized by an elaborate antioxidant defense system consisting of enzymes and numerous non-enzymatic antioxidants. Dietary antioxidant supplements are useful to counteract the carcinogenesis effects of arsenic. Oyster mushroom lectins can be regarded as ingredients of popular foods with biopharmaceutical properties. A variety of compounds have been isolated from mushrooms, which include polysaccharides and polysaccharopeptides with immune-enhancing effects. Lectins are beneficial in reducing arsenic toxicity due to anticarcinogenetic roles and may have therapeutic application in people suffering from chronic exposure to arsenic from natural sources, a global problem that is especially relevant to millions of people on the Indian subcontinent.

• The Korean Journal of Zoology
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• v.33 no.4
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• pp.476-492
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• 1990

Sodium arsenite (As) aqueous solution containing 4 ppm wss given to male rats for 15 days as drinking water. Electrophoretic pattern of liver cytosol from As-fed rats appeared to be significantly different from that of the control rats. Although the normal protein content of the cytosol fraction of As-fed rat liver was decreased, 8 stress proteins were increased. In liver cytosol fractions of As-treated rat, one kind of arsenic-binding substance (AsBS) was observed. Molecular weight of AsBS was identified to be 500 D and composition of amino acid was glycine, glutamic acid and cysteine. Glutathione (GSH) appeared to bind to arsenic and GSH-As complex showed the same mobility as AsBS on gel filtration chromatography. GSH conjugated As prevented As from inhibiting respiration, conformational change and swelling-contration of mitochondria. According to the above results. it is concluded that in vfuo treated arsenic stimulated synthesis of stress protein, and arsenic-binding substance might be glutathione and have a protective role against arsenic toxicity.

• Nutrition Research and Practice
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• v.8 no.2
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• pp.220-226
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• 2014

BACKGROUND/OBJECTIVES: Arsenic, which causes human carcinogenicity, is ubiquitous in the environment. This study was designed to evaluate modulation of arsenic induced cancer by resveratrol, a phytoalexin found in vegetal dietary sources that has antioxidant and chemopreventive properties, in arsenic trioxide ($As_2O_3$)-induced Male Wistar rats. MATERIALS/METHODS: Adult rats received 3 mg/kg $As_2O_3$ (intravenous injection, iv.) on alternate days for 4 days. Resveratrol (8 mg/kg) was administered (iv.) 1 h before $As_2O_3$ treatment. The plasma and homogenization enzymes associated with oxidative stress of rat kidneys were measured, the kidneys were examined histologically and trace element contents were assessed. RESULTS: Rats treated with $As_2O_3$ had significantly higher oxidative stress and kidney arsenic accumulation; however, pretreatment with resveratrol reversed these changes. In addition, prior to treatment with resveratrol resulted in lower blood urea nitrogen, creatinine and insignificant renal tubular epithelial cell necrosis. Furthermore, the presence of resveratrol preserved the selenium content ($0.805{\pm}0.059{\mu}g/g$) of kidneys in rats treated with $As_2O_3$. However, resveratrol had no effect on zinc level in the kidney relative to $As_2O_3$-treated groups. CONCLUSIONS: Our data show that supplementation with resveratrol alleviated nephrotoxicity by improving antioxidant capacity and arsenic efflux. These findings suggest that resveratrol has the potential to protect against kidney damage in populations exposed to arsenic.

• Journal of Environmental Health Sciences
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• v.23 no.4
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• pp.9-15
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• 1997

This experiment was carried out to examine the roles of selenium in arsenic- and chromium-induced oxidative stress, which results in chromosomal damage, such as sister chromatid exchange (SCE) and chromosomal aberration (CA). For this purpose, the frequency of CA and SCE related to the level of 0xidative stress were analyzed. Selenium decreased the frequency of CA induced by As. In order to evaluate the effect of selenium on clastogenic factors, media from As- and Cr-treated cells were ultrafiltered and added again to cells in the presence or absence of selenium. Selenium decreased the frequency of SCE by As and Cr. This observation indicates the possibility of presence of clastogenic factor. In addition, the clastogenic factor would be involed in oxidative stress since selenium decreased the level of oxidative stress. Thus, it is suggested that selenium may play a role as an anti-clastogenic effector by preventing the oxidative stress, thereby decreasing the frequency of Asand Cr-induced chromosomal damage.

• Nutrition Research and Practice
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• v.8 no.1
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• pp.46-53
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• 2014

Inorganic arsenic (iAs) is a toxic metalloid found ubiquitously in the environment. In humans, exposure to iAs can result in toxicity and cause toxicological manifestations. Arsenic trioxide ($As_2O_3$) has been used in the treatment for acute promyelocytic leukemia. The kidney is the critical target organ of trivalent inorganic As ($iAs^{III}$) toxicity. We examine if oral administration of astaxanthin (AST) has protective effects on nephrotoxicity and oxidative stress induced by $As_2O_3$ exposure (via intraperitoneal injection) in rats. Markers of renal function, histopathological changes, $Na^+-K^+$ ATPase, sulfydryl, oxidative stress, and As accumulation in kidneys were evaluated as indicators of $As_2O_3$ exposure. AST showed a significant protective effect against $As_2O_3$-induced nephrotoxicity. These results suggest that the mechanisms of action, by which AST reduces nephrotoxicity, may include antioxidant protection against oxidative injury and reduction of As accumulation. These findings might be of therapeutic benefit in humans or animals suffering from exposure to $iAs^{III}$ from natural sources or cancer therapy.