Copper- and arsenate-induced oxidative stress in Holcus lanatus L. clones with differential sensitivity

The biochemical responses of Holcus lanatus L. to copper and arsenate exposure were investigated in arsenate‐tolerant and ‐non‐tolerant plants from uncontaminated and arsenic/copper‐contaminated sites. Increases in lipid peroxidation, superoxide dismutase (SOD) activity and phytochelatin (PC) production were correlated with increasing copper and arsenate exposure. In addition, significant differences in biochemical responses were observed between arsenate‐tolerant and ‐non‐tolerant plants. Copper and arsenate exposure led to the production of reactive oxygen species, resulting in significant lipid peroxidation in non‐tolerant plants. However, SOD activity was suppressed upon metal exposure, possibly due to interference with metallo‐enzymes. It was concluded that in non‐tolerant plants, rapid arsenate influx resulted in PC production, glutathione depletion and lipid peroxidation. This process would also occur in tolerant plants, but by decreasing the rate of influx, they were able to maintain their constitutive functions, detoxify the metals though PC production and quench reactive oxygen species by SOD activity.     

Arsenic toxicity is not due to a direct effect on the oxidation of reduced inorganic sulfur compounds by Thiobacillus caldus

Abstract Thiobacillus caldus is a moderately thermophilic acidophile which has been implicated in the biooxidation of arsenic containing mineral Sulfides. The toxic effects of arsenic on this bacterium are presented here. Addition of arsenite to a growing culture of T. caldus caused a transient increase in the optical density of the culture while causing a simultaneous decrease in cell viability. The increase in optical density was shown to be due to the formation of extracellular sulfur. The oxidation rates of tetrathionate and thiosulfate were decreased by increasing concentrations of arsenite, while in a culture induced to arsenic resistance the rates were not as adversely effected. Sulfur oxidation was also inhibited to the same extent as tetrathionate oxidation, with the oxidation of solid sulfur being slightly more effected than the oxidation of sulfur dissolved in acetone. Thus, bactericidal arsenite causes a transient formation of extracellular sulfur in the culture supernatant of T. caldus yet the toxicity of arsenite is not due to direct inhibitory effects on reduced inorganic sulfur compound oxidation by these bacteria.     

Chemical and biological pathways in the bacterial oxidation of arsenopyrite

Abstract: A moderately thermophilic mixed culture of bacteria catalysed the oxidative solubilization of arsenopyrite to give Fe(III), S(VI) and As(V). Toxic effects were observed in a few experiments due to teh build-up of As(III). The bacterial oxidation of arsenopyrite involved direct attack of the bacteria on the mineral to give AS(III). Subsequent oxidation of AS(III) to AS(V) occurred reaction with FE(III), but only in the presence of pyrite, which provide a catalytic surface. Arsenopyrite was unable to act as a catalyst. The pyrite- catalysed oxidation of As(III) to AS(V) by FE(III) usually only went to completion in the presence of bacteria, possibly due to their role in the provision of clean catalytic surfaces. Thus, toxic concentrations of As(III) may accumulate in reactors during the bacterial oxidation of arsenopyrite due to the absence of pyrite or a clean pyrite surface or to low concentrations of the effective oxidizing agent, Fe(III).     

Essential trace elements in humans

Serum arsenic concentrations of persons suffering from renal failure and undergoing hemodialysis treatment (n=85) and of healthy controls (n=25) were determined by hydride-generation AAS technique after microwave digestion. The results were evaluated by comparing the values of both groups, considering physiological factors and individual data, as well as comorbid conditions of the hemodialysis (HD) patients. Serum arsenic levels were diminished in the patient group compared with controls (mean values 8.5±1.8 ng/mL vs 10.6±1.3 ng/mL). Furthermore, additional diseases within the hemodialysis group, particularly injuries of the central nervous system (CNS), vascular diseases, and cancer, were correlated to occasionally markedly decreased serum arsenic concentrations. It was concluded that arsenic homeostasis is disturbed by HD treatment and certain additional diseases. Desirable arsenic concentrations in the body seem to be reasonable. This consideration results in the conclusion that arsenic could play an essential role in human health. Thus, reference arsenic concentrations in different human tissues and body fluids should be established in order to recognize not only arsenic intoxication, but also arsenic deficiency. Perhaps arsenic deficiency contributes to the increased death risk of HD patients, and therefore, arsenic supplementations for patients with extremely low serum arsenic concentrations should be taken into account.     

Exposure of preterm neonates to toxic metals during their stay in the Neonatal Intensive Care Unit and its impact on neurodevelopment at 2 months of age

BackgroundPremature neonates might be exposed to toxic metals during their stay in the neonatal intensive care unit (NICU), which could adversely affect neurodevelopment; however, limited evidence is available. The present study was therefore designed to assess the exposure to mercury, lead, cadmium, arsenic, and manganese of preterm neonates who received total parenteral nutrition (TPN) and/or red blood cell (RBC) transfusions during their NICU stay and the risk of neurodevelopment delay at the age of 2 months.MethodsWe recruited 33 preterm neonates who required TPN during their NICU admission. Blood samples were collected for metal analysis at two different time points (admission and before discharge). Metals in the daily TPN received by preterm neonates were analyzed. Neurodevelopment was assessed using the Ages and Stages Questionnaire Edition 3 (ASQ-3).ResultsAll samples of TPN had metal contamination: 96% exceeded the critical arsenic limit (0.3 μg/kg body weight/day); daily manganese intake from TPN for preterm neonates exceeded the recommended dose (1 µg/kg body weight) as it was added intentionally to TPN solutions, raising potential safety concerns. All samples of RBC transfusions exceeded the estimated intravenous reference dose for lead (0.19 µg/kg body weight). Levels of mercury, lead and manganese in preterm neonates at discharge decreased 0.867 µg/L (95% CI, 0.76, 0.988), 0.831 (95%CI, 0.779, 0.886) and 0.847 µg/L (95% CI, 0.775, 0.926), respectively. A decrease in ASQ-3-problem solving scores was associated with higher levels of blood lead in preterm neonates taken at admission (ß = −0.405, 95%CI = −0.655, −0.014), and with plasma manganese (ß = −0.562, 95%CI = −0.995, −0.172). We also observed an association between decreased personal social domain scores with higher blood lead levels of preterm neonates before discharge (ß = −0.537, 95%CI = −0.905, −0.045).ConclusionOur findings provide evidence to suggest negative impacts on the neurodevelopment at 2 months of preterm infants exposed to certain metals, possibly related to TPN intake and/or blood transfusions received during their NICU stay. Preterm neonates may be exposed to levels of metals in utero.     

Comutagenesis of sodium arsenite with ultraviolet radiation in Chinese hamster V79 cells

Summary Solar ultraviolet radiation has been associated with the induction of skin cancer. Recent studies have indicated that near-ultraviolet, especially UVB, is mutagenic. Exposure to trivalent inorganic arsenic compounds has also been associated with increased skin cancer prevalence. Trivalent arsenic compounds are not mutagenicper se, but are comutagenic with a number of cancer agents. Here, we test the hypothesis that arsenite enhances skin cancer via its comutagenic action with solar ultraviolet radiation. Irradiation of Chinese hamster V79 cells with UVA (360 nm), UVB (310 nm) and UVC (254 nm) caused a fluence-dependent increase in mutations at thehprt locus. On an energy basis, UVC was the most mutagenic and UVA the least. However, when expressed as a function of toxicity, UVB was more mutagenic than UVC. Nontoxic concentrations of arsenite increased the toxicity of UVA, UVB and UVC. Arsenite acted as a comutagen at the three wavelengths; however, higher concentrations of arsenite were required to produce a significant (P < 0.05) comutagenic response with UVB. The increased mutagenicity of UVB and UVA by arsenite may play a role in arsenite-related skin cancers.     

Arsenic in orchard and potato soils and plant tissue

Summary The total and water soluble arsenic contents of orchard and potato field soils are significantly higher where arsenic has been applied. Orchards with a record of past and present applications show average values as high as 99.57 ppm total arsenic and 1.99 ppm water-soluble arsenic. Orchards with a low or no arsenic application show 27.21 ppm total and 0.20 ppm water-soluble arsenic. Potato fields situated on ex-orchard plantings have an average of 38.70 ppm total and 0.32 ppm water-soluble arsenic, whereas those on non-orchard soils showed values of 9.63 and 0.04 ppm respectively. Highest soil arsenic concentrations were found in the 0–10 cm surface layer and at a distance of one meter from the tree trunk. In plant tissue the apple leaf, peel and pulp all were significantly higher for recently arsenic treated orchards, while only the apple pulp showed significance where applications had been discontinued for the past 10–15 years. Potato leaf and peel were significantly higher in arsenic on exorchard soil while the pulp was not.