PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “ARSENIC AND COMPOUNDS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources
PubMed2003

Protective role of ascorbic acid and alpha-tocopherol on arsenic-induced microsomal dysfunctions.

Arsenic, a naturally occurring element, is present in food, soil, air and water. All human populations are exposed to arsenic and its compounds through occupational or environmental processes. Since arsenic compounds have been shown to exert their toxicity chiefly by generating reactive oxygen species, we have evaluated the effect of ascorbic acid and alpha-tocopherol on oxidative damage, antioxidant status and on xenobiotic metabolizing systems in arsenic-exposed rat liver and kidney microsomes. Arsenic exposure increases oxidative damage to lipids and proteins and decreases the levels of antioxidants and the activities of xenobiotic metabolizing enzymes. Coadministration of ascorbic acid and alpha-tocopherol to arsenic-exposed rats resulted in a reduction in the levels of lipid peroxidation, protein carbonyls and hydrogen peroxide and an elevation in the levels of reduced glutathione, ascorbic acid and alpha-tocopherol. Ascorbic acid and alpha-tocopherol treatment decreases the activity of haem oxygenase, whereas it increases the levels/ activity of cytochrome P450, cytochrome b5 and NADPH-cytochrome P450 reductase in arsenic-intoxicated rats. The results of this study provide evidence that ascorbic acid and alpha-tocopherol supplementation can improve the arsenic-induced altered microsomal functions in liver and kidney.

Animals↗
PubMed2003

Purification and characterization of thiols in an arsenic hyperaccumulator under arsenic exposure.

Pteris vittata (Chinese brake fern) is the first reported arsenic hyperaccumulator. To investigate the arsenic tolerance mechanism in this plant, reversed-phase HPLC with postcolumn derivatization was used to analyze the thiols induced under arsenic exposure. A major thiol in the plant leaflets was found to be responsive to arsenic exposure. The arsenic-induced compound was purified on a large scale by combining covalent chromatography and preparative reversed-phase HPLC. About 2 mg of this compound was isolated from 1 kg of fresh leaflets. The purified arsenic-induced compound was characterized using electrospray ionization mass spectrometry. A molecular ion (M + 1) of 540 and fragments were obtained, which indicated that the arsenic-induced thiol was a phytochelatin with two subunits (PC(2)). Compared to the classical methods for purification of phytochelatins, this new method is more specific, simple, and rapid and is suitable for purification of PCs in a large scale as well as sample preparation for mass spectrometry analysis.

Journal Article↗
PubMedDate not supplied

Synergistic toxicity between arsenic and methylated selenium compounds.

Arsenite has been known for half a century to have a protective effect against selenium poisoning. Paradoxically, arsenite inhibits the conversion of inorganic selenium salts to methylated excretory products, although methylation has long been regarded as a detoxification mechanism for selenium. Moreover, there is evidence for a pronounced synergistic toxicity between arsenite and methylated selenium metabolites. We investigated the effect of arsenite on the acute toxicity of a variety of methylated or nonmethylated selenium compounds, as well as methylated forms of sulfur and tellurium. Adult male rats were injected with sodium arsenite (4 mg As/kg bw, s.c.) 10 min prior to injection of the test compounds; at the doses employed, none of the test compounds caused mortality, nor did arsenite, when given alone. When given with arsenite, the following methylated compounds produced toxic signs and high morality at the indicated dosages (mg Se/kg): Methylseleninic acid (2), dimethylselenoxide (2), trimethylselenonium chloride (3), selenobetaine (2), selenobetaine methylester (2, also 1 and 0.5), and Se-methylselenocysteine (2). Toxic signs but not mortality occurred when arsenite was given with selenomethionine (2 mg Se/kg). No enhancement of toxic signs or mortality occurred when arsenite was given with sulfobetaine (0.8 mg S/kg), dimethylsulfide (320 mg S/kg), or the following (nonmethylated) forms of selenium: sodium selenite (2), selenocystine (2), and phenylselenol (2). Arsenite also increased the toxicity of trimethyltelluronium chloride (4.8 mg Te/kg). Like arsenite, periodate-oxidized adenosine (100 mumoles/kg), which is known to inhibit the formation of dimethylselenide and trimethylselenonium ion in vivo, caused increased 24 h mortality when given with various methylated selenium compounds.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

National Human Exposure Assessment Survey (NHEXAS): distributions and associations of lead, arsenic and volatile organic compounds in EPA region 5.

The National Human Exposure Assessment Survey (NHEXAS) Phase I field study conducted in EPA Region 5 provides extensive exposure data on approximately 250 study participants selected via probability sampling. Associated environmental media and biomarker (blood, urine) concentration data were also obtained to aid in the understanding of relationships of the exposures to both contaminant sources and doses. Distributional parameters for arsenic (As), lead (Pb), and four volatile organic compounds (VOCs)--benzene, chloroform, tetrachloroethylene, and trichloroethylene--were estimated for each of the relevant media using weighted data analysis techniques. Inter-media associations were investigated through correlation analysis, and longitudinal correlations and models were used to investigate longitudinal patterns. Solid food appeared to be a major contributor to urine As levels, while Pb levels in household (HH) dust, personal air, and beverages all were significantly associated with blood Pb levels. Relatively high (>0.50) longitudinal correlations were observed for tap water Pb and As, as compared to only moderate longitudinal correlations for the personal air VOCs.

Arsenic↗
PubMed2004

[Occupation related thoracic tumors].

It is estimated that about 4% of cancer mortality is attributed to occupational risk factors. Due to long latency periods it is often difficult to establish causal relationships. Thoracal cancer accounts for about 88% of all compensated occupational cancers in Germany. Most important exposures and diseases are asbestos-related lung cancer, asbestos-related malignant mesothelioma and radiation induced lung cancer (by Radon and its decay products). Lung cancer caused by nickel compounds, hexavalent chromium, arsenic and its compounds, coke oven gases and polycyclic aromatic hydrocarbons are rare. Silica-dust induced lung cancer can be compensated as occupational disease if a silicosis is present. In Germany every physician is obliged to notify a suspected occupational cancer as well as other occupational diseases.

Asbestosis↗
PubMed1988

Chemical speciation and distribution of arsenic in water, suspended solids and sediment of Xiangjiang River, China.

The forms of arsenic in the Zuzou Zone of the Xiangjang River are evaluated. Nine fractions of arsenic, consisting of soluble arsenic(III) and total soluble arsenic, loosely bound arsenic, aluminium arsenate, iron arsenate, calcium arsenate, arsenic occluded on iron oxide, organic compounds of arsenic and residual arsenic, were separated from suspended solids and sediments by sequential chemical extraction. All arsenic fractions were determined by ASV and AFS. The distributions of arsenic and arsenic fractions in water, sediments and suspended solids are discussed in terms of the mechanisms of arsenic transport and deposition in aquatic ecosystems.

Arsenic↗
PubMedDate not supplied

Carcinogenic and systemic health effects associated with arsenic exposure--a critical review.

Arsenic and arsenic containing compounds are human carcinogens. Exposure to arsenic occurs occupationally in several industries, including mining, pesticide, pharmaceutical, glass and microelectronics, as well as environmentally from both industrial and natural sources. Inhalation is the principal route of arsenic exposure in occupational settings, while ingestion of contaminated drinking water is the predominant source of significant environmental exposure globally. Drinking water contamination by arsenic remains a major public health problem. Acute and chronic arsenic exposure via drinking water has been reported in many countries of the world, where a large proportion of drinking water is contaminated with high concentrations of arsenic. General health effects that are associated with arsenic exposure include cardiovascular and peripheral vascular disease, developmental anomalies, neurologic and neurobehavioural disorders, diabetes, hearing loss, portal fibrosis, hematologic disorders (anemia, leukopenia and eosinophilia) and multiple cancers: significantly higher standardized mortality rates and cumulative mortality rates for cancers of the skin, lung, liver, urinary bladder, kidney, and colon in many areas of arsenic pollution. Although several epidemiological studies have documented the sources of exposure and the global impact of arsenic contamination, the mechanisms by which arsenic induces health effects, including cancer, are not well characterized. Further research is needed to provide a better understanding of the pathobiology of arsenic-induced diseases and to better define the toxicologic pathology of arsenic in various organ systems. In this review, we provide and discuss the underlying pathology and nature of arsenic-induced lesions. Such information is critical for understanding the magnitude of health effects associated with arsenic exposure throughout the world.

Arsenic↗
PubMed1981

Sources, transport and alterations of metal compounds: an overview. I. Arsenic, beryllium, cadmium, chromium, and nickel.

An overview is presented of the current state of knowledge of the salient aspects of the sources, transport, and alterations of arsenic, beryllium, cadmium, chromium, and nickel. This information is considered vital for a better assessment of the scope of potential human hazard to these ubiquitous toxicants and their compounds. Stress is focused on both natural and industrial activities, particularly on the latter's projected trends. Increasing use patterns per se of most of these metals, as well as aspects of waste disposal and the anticipated increased combustion of fossil fuels for power generation and space heating (particularly in the United States), are major causes of potential health concern. Additionally, attention is drawn to the need for increased research to fill the gaps in our knowledge in these vital areas, all in the hope of permitting a more facile identification and quantification of the potential hazard to exposure to these agents.

Air Pollutants↗
PubMed1964

INDUCTION AND MECHANISMS OF ARSENITE RESISTANCE IN PSEUDOMONAS PSEUDOMALLEI.

Arima, Kei (University of Tokyo, Tokyo, Japan), and Michiko Beppu. Induction and mechanisms of arsenite resistance in Pseudomonas pseudomallei. J. Bacteriol. 88:143-150. 1964.-Pseudomonas pseudomallei strain 54, able to grow in the presence of 2 x 10(-2)m arsenite, was isolated from soil. After a short lag period, it grew at a normal growth rate. In the organisms grown with 10(-2)m arsenite, oxidation of alpha-ketoglutarate and other substrates proceeded in the presence of the same concentration of the drug. The concentration of arsenite which was half-inhibitory to alpha-ketoglutarate oxidation was 1.6 x 10(-3)m in the sensitive bacteria and 3.3 x 10(-2)m in the resistant ones. Cells capable of oxidizing alpha-ketoglutarate in the presence of arsenite were induced rapidly by contact with arsenite in growing cultures; when the drug was removed from the cultures, resistance was maintained for about two generations and then gradually disappeared. From the data presented, it was concluded that resistance in this organism is a physiological change and not a hereditary one. Further studies were carried out to investigate the arsenite-resistance mechanisms. alpha-Ketoglutarate dehydrogenase activity in the cell-free extracts of the resistant bacteria was sensitive to arsenite. An increase in the contents of this enzyme and sulfhydryl compounds, involving lipoic acid, was not observed in the resistant bacteria. The possibility of detoxication of arsenite was ruled out. Treatment of the resistant cells with cetyl-trimethylammonium bromide made them susceptible to 2 x 10(-2)m arsenite, although untreated cells were resistant to the same concentration of the drug. These data suggest the decreased permeability to arsenite of the resistant bacteria as a main mechanism of resistance.

Ammonium Compounds↗
PubMed1998

Fungal volatilization of arsenic and antimony and the sudden infant death syndrome.

Fungal volatilization of antimony and other group Vb elements has been proposed to have a causal role in the sudden infant death syndrome (SIDS; cot death). The ability of fungi to produce volatile arsenic and antimony compounds in pure culture was examined using Scopulariopsis brevicaulis, reported as an inhabitant of PVC cot mattress covers, and Phaeolus schweinitzii, a wood decay fungus known to be a good volatilizer of arsenic. Volatile arsenic compounds were detected from all cultures grown on arsenic-supplemented media, but antimony volatilization was not reliably detected. Although antimony levels above the baseline sensitivity of the analytical technique were detected in four (out of 24) of the samples analyzed, the concentrations recorded were too low to be reliably interpreted as evidence for volatilization. Our results are discussed in relation to hypotheses regarding the causes of SIDS.

Antimony↗