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PubMed2005

Assessment of arsenic contamination of groundwater and health problems in Bangladesh.

Excessive amounts of arsenic (As) in the groundwater in Bangladesh and neighboring states in India are a major public health problem. About 30% of the private wells in Bangladesh exhibit high concentrations of arsenic. Over half the country, 269 out of 464 administrative units, is affected. Similar problems exist in many other parts of the world, including the Unites States. This paper presents an assessment of the health hazards caused by arsenic contamination in the drinking water in Bangladesh. Four competing hypotheses, each addressing the sources, reaction mechanisms, pathways, and sinks of arsenic in groundwater, were analyzed in the context of the geologic history and land-use practices in the Bengal Basin. None of the hypotheses alone can explain the observed variability in arsenic concentration in time and space; each appears to have some validity on a local scale. Thus, it is likely that several biogeochemical processes are active among the region's various geologic environments, and that each contributes to the mobilization and release of arsenic. Additional research efforts will be needed to understand the relationships between underlying biogeochemical factors and the mechanisms for arsenic release in various geologic settings.

Arsenic↗
PubMed2006

Inorganic arsenic in drinking water and bladder cancer: a meta-analysis for dose-response assessment.

Most arsenic cancer risk assessments have been based solely on epidemiological studies to characterize the dose-response relationship for arsenic-associated cancer and to perform risk calculations. However, current epidemiological evidence is too inconsistent and fraught with uncertainty regarding arsenic exposure to provide reliable estimates. This makes it hard to draw a firm conclusion about the shape and slope of the dose-response relationship from individual studies. Meta-analysis is a statistical approach to combining results across studies and offers expanded opportunities for obtaining an improved dose-response relationship. In this study, a meta-analysis of arsenic studies was conducted by combining seven epidemiological studies from different regions to get an overall dose-response relationship between the amount of arsenic intake and the excess probability of bladder cancer. Both the fixed-effect and random-effect models were used to calculate the averaged coefficient of the linear-logistic regression model. A homogeneity test was also conducted. The final product of this research is an aggregated dose-response model in the range of empirical observation of arsenic. Considering the most recent arsenic MCL (maximum contaminant level, i.e. 10microg/L), the associated bladder cancer risk (lifetime excess probability) at this MCL is 2.29 x 10-5.

Arsenic↗
PubMedDate not supplied

Arsenic trioxide inhibits proliferation and induces apoptosis in pancreatic cancer cells.

Because of the poor therapeutic responsiveness of pancreatic cancer patients, new chemotherapeutic agents for pancreatic cancer would be extremely beneficial. The effects of arsenic trioxide in pancreatic cancer have not been explored. To evaluate the anti-pancreatic cancer effects of arsenic trioxide, three human pancreatic cell lines, HPAF, MiaPaCa-2 and PANC-1, were tested. Arsenic trioxide caused dose- and time dependent inhibition of pancreatic cancer cell proliferation. In parallel with inhibition of cell proliferation, arsenic trioxide induced significant morphological changes, including shrunken cytoplasm, membrane blebbing, and nuclear condensation consistent with apoptosis. Propidium iodide DNA staining showed an increase of the sub-G0/G1 cell population. The DNA fragmentation induced by arsenic trioxide in these three cell lines was confirmed by the TUNEL assay. Furthermore, Western blotting analysis indicated that caspase-3 was activated following arsenic trioxide as measured by procaspase-3 cleavage and PARP cleavage. These findings show that arsenic trioxide has potent anti-proliferative effects on human pancreatic cancer cells with induction of apoptosis in vitro.

Antineoplastic Agents↗
PubMed2002

[Research advances on effect of arsenic trioxide on tumor].

Arsenic compounds are natural substances that have been used medically for more than 2,400 years in China. Since 1990s, Chinese physicians have began to use arsenic trioxide in treating the patients with acute promyelocytic leukemia (APL), and the results showed that arsenic trioxide was effective on APL patients. Further study of arsenic trioxide demonstrated that arsenic trioxide was safe and effective not only on patients with leukemia, but also on patients with many other kinds of malignant cancers. Arsenic trioxide exerted its anti-cancer effects mainly by inhibiting the cell growth and angiogenesis, inducing the cell partial cytodifferentiation and apoptosis, etc. In addition, this review looked forward to the prospect of application of gene chip, a newly developed and powerful technology in analysis of gene expression profile, in elucidation of the mechanism of arsenic trioxide on tumor.

Antineoplastic Agents↗
PubMed2003

A cheap and convenient modification of arsine generator used for arsenic estimation.

In a study observing the effect of spirulina in the treatment of chronic arsenic poisoning quantitative estimation of arsenic in the urine of the patients was necessary. It was decided to try a modification of the arsine generator in the process. An alternative apparatus was designed following the structure of arsine generator by White (1976) using a 50-ml conical flask with rubber cork, 4-ml injection vial, two 3" long glass tubes and a glass test tube. An experiment was carried out with solutions containing known amounts of arsenic. The alternative arsine generator was tried in the estimation of arsenic content in those solutions. The results revealed that the apparatus permitted correct measurement of arsenic concentration. The alternative arsine generator was cheap easy to use and provided authentic results in estimation of arsenic concentration in the urine of patients with chronic arsenic poisoning.

Arsenic Poisoning↗
PubMed2003

[Effect of arsenic trioxide on rabbit vascular smooth muscle cells after balloon angioplasty].

OBJECTIVE: To study the apoptotic effect of arsenic trioxide on rabbit vascular smooth muscle cells (RVSMCs) after balloon angioplasty. METHODS: A New Zealand rabbit underwent balloon angioplasty three times at one of its iliac arteries. The iliac artery at the opposite side was used as control. Three days after the rabbit was killed. The VSMCs of the iliac artery undergoing balloon angioplasty were cultured. Arsenic trioxide of different concentrations was added into the culture. VSMCs not co-incubated with arsenic trioxide was used as controls. Cell proliferation curve was drawn. DNA was extracted and underwent electrophoresis. Transmission electron microscopy was used to observe the ultramicroscopic structure. TUNEL technique was used to examine the apoptosis of cells. RESULTS: Cell proliferation curve showed that the control cells grew geometrically and reached a plateau stage by day 3. The cells co-incubated with arsenic trioxide proliferated more slowly and the plateau stage appeared earlier dose-dependently (P < 0.05). Electrophoresis showed obscure ladder band of DNA specific to cell apoptosis, especially at the concentrations of arsenic trioxide of 3.0 and 4.0 micro mol/L. Transmission electron microscopy showed apoptotic cells with apoptosis nodes. TUNEL technique showed that the number of yellow-dyed cells was significantly larger after the addition of arsenic trioxide. The above-mentioned manifestations were not seen in the control group. CONCLUSION: Arsenic trioxide increases the apoptosis of rabbit vascular smooth muscle cells after balloon angioplasty and inhibits RVSMCs over-proliferation. It is a hopeful measure in prevention of re-stenosis after angioplasty.

Angioplasty, Balloon↗
PubMed2003

[Construction of subtracted cDNA library in human Jurkat T cell line induced by arsenic trioxide in vitro].

OBJECTIVE: To understand the differentially expressed genes in human T lymphocytes induced by arsenic trioxide (As(2)O(3)) and to explore mechanism of its immunotoxicity and immune suppression. METHODS: Human Jurkat T cell line was treated by arsenic trioxide (5 micromol/L, 24 h) in vitro, as a sample model. Then, the differentially expressed genes were cloned and the subtractive cDNA library from Jurkat T cell line was constructed by suppression subtractive hybridization (SSH). Polymerase chain reaction (PCR) and sequencing techniques were applied to identify positive clones. RESULTS: The forward subtracted cDNA library contained differentially expressed genes from Jurkat T cell line induced by arsenic trioxide was constructed, including 29 different gene fragments and only replicated one in the subtracted cDNA library identified by PCR and sequencing analysis. These gene sequences were 95%-100% analogous to the genes in public database (GenBank/EMBL). The cDNA library contained oxidative metabolic genes in mitochondria (triose phosphate dehydrogenase, NADH4, pyrophosphate synthase, 16S rRNA ribosome, succinate-CoA ligase and ATP synthase 6); transcriptional and translation genes poly (A) binding protein, t-RNA-guanine transglycoslase, ribosomal protein L23, ribosomal protein S15A, eukaryotic translation initiation factor 3, Rab interaction protein 5, splicing factor-arginine serine rich 5, and ADP-ribosylation factor-like 6 interacting protein), oxide stress related genes (ferritin high chain and high-mobility group protein 2); protein activating and signaling pathway related genes (casein kinase, serine kinase 2 and phosphatidylinositol-four-phosphate adaptor protein-1-associated protein); cell differentiation and apoptosis associated genes (NB4 cell apoptosis related protein and myeloid differentiation primary response protein) and five genes with unknown function (KIAA0092, CGI-147protein, GCI-35, nucleolar phosphoprotein Nopp34 and Mus muscular partial mRNA for hypothetical protein), as well as a novel gene unmatched to the sequence in GenBank. CONCLUSIONS: The forward subtracted cDNA library contained differentially expressed genes from Jurkat T cell line induced by arsenic trioxide was successfully constructed. And, genes not involved in previous research on arsenic were found. Results of analysis for these genetic function suggested that there should be many genes involved in process of T lymphocytes apoptosis or injury induced by arsenic trioxide and that there should still be many genes associated with arsenic that were not reported in the past.

Antineoplastic Agents↗
PubMed2003

[Absorption and distribution of mercury and arsenic from realgar and cinnabar of angong niuhuang pill in normal rats and rats with cerebral ischemia].

OBJECTIVE: To study comparatively the characteristics of absorption and distribution of mercury and arsenic from realgar and cinnabar of Angong Niuhuang Pill in normal rats and the rats with cerebral ischemia after oral administration. METHOD: The blood samples and homogenates of liver, kidney and brain were prepared at various intervals after the animals were treated with Angong Niuhuang pill ig. The levels of total mercury and total arsenic in the blood and the organ homogenates were measured with Microwava Accelerated Reaction System and AAs, respectively. RESULT: The blood concentrations of mercury and arseic reached the highest point in normal rats at one hour following single oral dosing of Angong Niuhuang pill. In normal rats, the mercury distribution was characterized by its higher level in blood and kidneys than in other organs, while a higher distribution of arsenic was found in blood than in organs. No difference in the distribution of mercury or arsenic was found between normal rats and rats with cerebral ischemia after the treatment with the pill. CONCLUSION: The highest level of mercury or arsenic in blood occurs at one hour after oral administration of the pill in normal rats. There is a higher distribution of mercury in blood and kidneys, while a higher distribution of the arsenic only in blood. There is no significant difference in the distribution of mercury or arsenic between the normal rats and the ischemic rats.

Animals↗
PubMedDate not supplied

[Acute polyneuropathy and encephalopathy caused by arsenic poisoning].

INTRODUCTION: Acute arsenic toxicity is a multisystemic disease with pleural and pericardial effusions, gastrointestinal symptoms and pancytopenia. The most frequent neurological complication of inorganic arsenic intoxication is a distal symmetrical polyneuropathy. CASE REPORT: We report here a patient who developed a systemic illness followed with severe acute polyneuropathy. Electrophysiological findings suggested a Guillain-Barré syndrome (GBS). Finally an acute encephalopathy appeared which led to reconsideration of the diagnosis. A 24-hour heavy metal urine, nail and hair analysis was performed. A diagnosis of arsenic toxicity was made. Instead of chelating therapy patient died due to respiratory failure. CONCLUSIONS: A misdiagnosis of GBS in inorganic arsenic polyneuropathy is not infrequent. Atypical progression compels to rule out arsenic or heavy metal intoxication. In our case the appearance of the encephalopathy was the key to the diagnosis. It has been suggested that axonal degeneration and segmental demyelination might be equally prominent pathological features of the neuropathy, depending on the dosage and the length of time of exposure to arsenic. The exact pathophysiology of arsenic polyneuropathy remains unclear and a interference with pyruvate oxidation has been postulated.

Arsenic↗
PubMed2004

[Effects of arsenic trioxide, ginseng saponin and beta-elemene on telomere-telomerase system in K562 cell line].

The aim was to explore the modulating and inhibiting effects of arsenic trioxide, ginseng saponin and beta-elemene on telomere length and telomerase activity in K562 cell line, and to study their anti-tumor mechanism and seek new method of therapy for acute leukemia. Human erythroleukemia cell line K562 was co-cultured with arsenic trioxide, ginseng saponin, beta-elemene separately, cells were collected after 24, 48 and 72 hours for further detecting. Telomere length and telomerase activity were detected by the methods of Southern-blot and PCR-ELISA respectively. The effects of these drugs on telomere length and telomerase activity were observed at different concentrations and length of time. The results showed that (1) telomerase activity of K562 cells decreased after co-cultured with arsenic trioxide, ginseng saponin and beta-elemene. The inhibiting effects depended on drug concentrations and length of time. When co-cultured at proper concentration and period of time, telomerase activity could be inhibited; (2) viability of K562 cells decreased after co-cultured with arsenic trioxide, ginseng saponin and beta-elemene, the inhibiting effect depends on drug concentrations and length of time; (3) after co-cultured with arsenic trioxide, ginseng saponin, and beta-elemene for 72 hours, telomere length of K562 cell line prolonged a little. It is concluded that (1) arsenic trioxide, ginseng saponin and beta-elemene can inhibit telomerase activity in K562 cell line, the suppression of telomerase activity may be one of the mechanisms of anti-tumor effect; (2) arsenic trioxide, ginseng saponin and beta-elemene can inhibit the growth of K562 cell line, the inhibiting effect depends on concentration and time; (3) when telomerase activity was suppressed, the telomere length prolonged a little, indicating that in K562 cell line may exist another mechanism to regulate telomere length, except telomerase activation.

Arsenic Trioxide↗
PubMed2006

Arsenic in drinking-water and reproductive health outcomes: a study of participants in the Bangladesh Integrated Nutrition Programme.

This study examined 2,006 pregnant women chronically exposed to a range of naturally-occurring concentrations of arsenic in drinking-water in three upazilas in Bangladesh to find out relationships between arsenic exposure and selected reproductive health outcomes. While there was a small but statistically significant association between arsenic exposure and birth-defects (odds ratio=1.005, 95% confidence interval 1.001-1.010), other outcomes, such as stillbirth, low birth-weight, childhood stunting, and childhood under-weight, were not associated with arsenic exposure. It is possible that the association between arsenic exposure from drinking-water and birth-defects may be a statistical anomaly due to the small number of birth-defects observed. Future studies should look more closely at birth-defects, especially neural tube defects, to elucidate any potential health effects associated with arsenic exposure from drinking-water. Further, given the knowledge that serious health effects can result from chronic arsenic exposure, efforts to find alternatives of safe drinking-water for the population must continue.

Abnormalities, Drug-Induced↗
PubMed2006

Association of arsenic-contaminated drinking-water with prevalence of skin cancer in Wisconsin's Fox River Valley.

During July 2000-January 2002, the Wisconsin Division of Public Health conducted a study in 19 rural townships. A high percentage of private drinking-water wells in these townships contained traces of arsenic. Residents were asked to collect well-water samples and complete a questionnaire regarding residential history, consumption of drinking-water, and family health. In total, 2,233 household wells were tested, and 6,669 residents, aged less than one year to 100 years, provided information on water consumption and health. The well-water arsenic levels ranged from less than 1.0 to 3,100 microg/L. The median arsenic level was 2.0 microg/L. The arsenic levels were below the federal drinking-water standard of 10 microg/L in 80% of the wells, while 11% had an arsenic level of above 20 microg/L. Of residents aged over 35 years, those who had consumed arsenic-contaminated water for at least 10 years were significantly more likely to report a history of skin cancer than others. Tobacco use was also associated with higher rates of skin cancer and appeared to synergize the effect of arsenic on the development of skin cancer.

Adult↗
PubMed1994

Human urinary arsenic excretion after one-time ingestion of seaweed, crab, and shrimp.

We studied chemical speciation of arsenic compounds in urine samples by using HPLC with inductively coupled plasma mass spectrometry detection. We examined urinary arsenic excretion patterns and the arsenic species excreted from nine human subjects who ingested seaweed products and crab (or shrimp). Fast urinary excretion of unchanged arsenobetaine was seen after ingestion of crab and shrimp, which contain arsenobetaine as the major arsenic species. In contrast, the arsenosugars, which comprise the major arsenic species in seaweed, are metabolized and have a longer retention time in the human body. When nine volunteers ingested the commercial seaweed product nori, both the urinary arsenic excretion pattern and the excreted arsenic species varied from individual to individual, and as many as six metabolites could be detected. It seems that arsenosugars are not decomposed by stomach acid and that reactions involving enzymatic and (or) microbial activity in the human body may be responsible for the metabolism of arsenosugars.

Adult↗
PubMed1997

Evaluation of a food frequency questionnaire-food composition approach for estimating dietary intake of inorganic arsenic and methylmercury.

Inorganic arsenic intake in 969 men and women and methylmercury intake in 785 men and women from across the United States were assessed by a semiquantitative food frequency questionnaire, in combination with a database for the content of those elements in foods, and by toenail concentrations of arsenic and mercury. In addition, empirical weights for foods on the dietary questionnaire were derived from multivariate regression models to estimate associations between diet and toenail arsenic and mercury levels, independent of the assumptions about inorganic arsenic and methylmercury in foods, which are based upon limited residue measurements. The use of empirical weights significantly improved the correlation of arsenic consumption with toenail arsenic levels (r = 0.33, P = 0.0001), compared with the weak correlation obtained using the food residue method to calculate intake (r = 0.15, P = 0.0001). Mercury consumption computed using empirical weights yielded a significant correlation with toenail arsenic (r = 0.42, P = 0.001), similar to the correlation using energy-adjusted intake calculated from food residue tables (r = 0.35, P = 0.001). These results illustrate the potential use of empirically derived weights for foods in estimating toenail levels of selected heavy metals and support the validity of published food residue data that are used to estimate mercury consumption.

Adult↗
PubMed1994

Effect of various antidotes on the biliary and intestinal excretion of arsenic in situ and into the feces in vivo in guinea-pigs after injection of As2O3.

The effect of various antidotes on the excretion of arsenic into the feces in vivo and on the biliary and enteric excretion in situ was investigated on segments of jejunum and colon in anesthetized guinea-pigs using the pendular perfusion technique, according to Henning and Forth (1982). In the in situ experiments guinea-pigs received As2O3 (0.02 mmol As(III)/kg) and 30 min later, British-Anti-Lewisite (BAL), dimercaptopropanesulfonic acid (DMPS), dimercaptosuccinic acid (DMSA) or 2,3-bis-(acetylthio)propanesulfonamide (BAPSA) (0.1 or 0.7 mmol/kg each) into the jugular vein. In the in vivo experiments guinea-pigs received As2O3 s.c. (same dose as above) and 30 min later the same antidotes (0.1 mmol/kg i.p.). The feces were collected for 24 h and the arsenic content measured. During the 60-min perfusion period the amount of arsenic excreted into the jejunum or colon was only 3% or 0.4% of the dose administered, respectively. Of the arsenic dose, 8% was found in the bile. None of the antidotes had an effect on the arsenic excretion into the jejunum or colon. No change in biliary excretion was found in animals treated with BAL, 0.1 or 0.7 mmol/kg, respectively. DMSA, BAPSA or DMPS, 0.1 mmol/kg, increased the biliary excretion of arsenic to 14, 33, or 43% of the dose administered and after 0.7 mmol/kg to 29, 37, or 42%, respectively. Furthermore, a significant increase (P > 0.05) was found for the bile/blood concentration ratio in the following order: control < BAL < DMSA < BAPSA approximately DMPS.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

The metabolism of arsenic in humans acutely intoxicated by As2O3. Its significance for the duration of BAL therapy.

The urinary excretion of inorganic arsenic and of its less toxic metabolites [monomethylarsonic acid (MMA) and dimethylarsinic acid (DM)] has been followed-up in five cases of acute oral intoxication by As2O3. In addition to supportive therapy all patients were given BAL. The proportion of the three species of urinary arsenic (inorganic, MMA, DMA) changes markedly with time. During the first 2 to 4 d after the intoxication, arsenic is excreted mainly as its unmetabolized inorganic form but this is rapidly followed-up by a progressive increase of the proportion excreted as MMA and DMA. The time at which the majority of arsenic is excreted as its organic metabolites depends on the severity of the intoxication but in all the cases, more than 95% of th excreted arsenic is in the organic form after 9 d, the dimethylated derivative being preponderant. Speciation of arsenicals in urine might be useful to determine the duration of BAL treatment.

Adult↗
PubMed1980

Mechanism of arsenic-induced inhibition of erythropoiesis in mice.

Anemia accompanies arsenic intoxication in man. The present studies were undertaken to clarify further the effects of arsenic on erythropoiesis. A dose-related inhibition of red cell 59 Fe incorporation and reticulocyte response was observed in normal mice treated with a single injection of arsenic. Arsenite was approximately two times as inhibitory as arsenate. The effects of arsenic on erythropoietin-induced erythroid differentation revealed a significant inhibitory effect on young, proliferating marrow nucleated erythroid precursor cells. More mature, nonproliferating nucleated erythr oid cells were resistant to the toxic action of arsenic. A dose-related inhibitory effect of arsenic on DNA synthesis was observed in fetal liver nucleated erythroid cells incubated with 3 H thymidine. Ineffective erythropoiesis as well as the megaloblastic morphology accompanying aberrant DNA synthesis -- manifestations of arsenic toxicity in man -- were not evident in the present studies.

Animals↗
PubMed2006

Exposure of mice to arsenic and/or benzo[a]pyrene does not increase the frequency of Aprt-deficient cells recovered from explanted skin of Aprt heterozygous mice.

Exposure to inorganic arsenic in drinking water is linked to cancer in humans, but the mechanism of arsenic-induced cancer is not clear. Arsenic is not a powerful point mutagen, but can cause chromosome malsegregation and mitotic recombination, two events that can cause loss of tumor suppressor alleles and thereby contribute to the evolution of cancerous cells. To determine whether arsenic increases the frequency of allele loss due to either malsegregation or mitotic recombination in vivo, Aprt(+/-) hybrid mice were exposed to sodium arsenite (10 mg/L) in their drinking water for 10 weeks. To determine whether arsenic enhances the action of a known mutagen, half of the arsenic-treated mice were exposed to benzo[a]pyrene (BaP) for 8 weeks by skin painting (500 nmoles/week). Cells were taken from painted dorsal skin and cultured in the presence of 2,6-diaminopurine (DAP), to select colonies lacking adenosine phosphoribosyl transferase (Aprt) activity. The frequency of DAP-resistant (DAP(r)) colonies varied substantially within the treatment groups, but there was no significant difference between the groups. Analysis of DNA from DAP(r) colonies suggested that mitotic recombination contributed to the loss of wild-type Aprt allele. Whether arsenic or BaP enhanced or diminished the frequency of this process could not be deduced from these data.

2-Aminopurine↗