Rate Of Mercury Uptake Research Articles

Prediction of mercury bioavailability to common carp (Cyprinus carpio L.) using the diffusive gradient in thin film technique

The mercury bioaccumulation by common carp (Cyprinus carpio L.) tissues (gills, skin, eyes, scales, muscle, brain, kidneys, liver, and spleen) and the capability of the diffusive gradient in thin film (DGT) technique to predict bioavailability of mercury for individual carp's tissues were evaluated. Carp and DGT units were exposed to increasing concentrations of mercury (Hg2+: 0 μg L−1, 0.5 μg L−1, 1.5 μg L−1 and 3.0 μg L−1) in fish tanks for 14 days. In the uncontaminated fish group, the highest mercury concentration was determined in the muscle tissues and, in fish groups exposed to mercury, the highest mercury concentration was determined in the detoxification (kidneys) and input (gills) organs. A strong and positive correlation between the rate of mercury uptake by the DGT technique and the rate of mercury accumulation by fish tissues (gills, skin, scales, and eyes) was observed.

Kinetics of Vapor-Phase Mercury Uptake by Virgin and Sulfur-Impregnated Activated Carbons

ABSTRACT The injection of powdered activated carbon (PAC) into combustion flue gas, with subsequent collection in a particulate control device, and granular activated carbon (GAC) fixed-bed adsorption offer new promise for achieving high-quality air emissions with respect to elemental mercury concentrations. One of the key parameters that governs the applicability of adsorption technology to flue gas cleanup is the rate of vapor-phase mercury removal, which was the main focus of this study. The kinetics of vapor-phase mercury uptake by a virgin bituminous coal-based activated carbon (BPL), a commercially available sulfur impregnated activated carbon (HGR), and a BPL carbon impregnated with sulfur at 600 oC (BPL-S) was evaluated as a function of temperature and elemental mercury concentration. For all three carbons, an increase in mercury concentration and a decrease in temperature resulted in an increased overall mercury uptake. The rate of mercury uptake by HGR carbon was slower at higher temperatures due to the change in sulfur structure, which induced a decreased number of terminal sulfur atoms available to react with mercury. For a given flue gas temperature, an increase in mercury concentration resulted in slower mercury uptake kinetics, which suggests that the rate of mercuric sulfide (HgS) diffusion into the sulfur mass is the rate-limiting step. The rate of mercury uptake by BPL-S carbon deteriorated with an increase in temperature, which indicates that the rate of HgS formation is the rate-limiting step in the overall mercury removal process. BPL-S carbon displayed faster uptake kinetics and higher total mercury uptake than HGR carbon, except for very high initial mercury concentrations (e.g., >1,000 mg/m3 ).

Mercury bioaccumulation by shrimp ( Penaeus aztecus) transplanted to Lavaca Bay, Texas

A field study was conducted to determine mercury accumulation rates by brown shrimp, Penaeus aztecus, transferred to a mercury contaminated estuary, Lavaca Bay, Texas. Mercury levels in the caged shrimp rose from an average baseline value of 347 ± 163 ppb to 1170 ± 107 ppb in 36 days, resulting in an average rate of mercury uptake of 22 ppb per day. Our results show that shrimp rapidly accumulate Hg when confined to a contaminated area, even though the natural population of shrimp in Lavaca Bay is not contaminated.

Effects of endogenous and exogenous thiols on the distribution of mercurial compounds in mouse tissues.

The distribution of mercury, a well known environmental contaminant, has been evaluated in detail in several species of animals; however, limited information is available in the mouse. Considerable species differences exist in the distribution of various forms of mercury. In the current study, methylmercuric chloride or mercuric chloride were injected ip in mice at two dose levels. The concentration of mercury in various organs was determined by cold-vapor atomic absorption spectrometry. After the administration of methylmercury, the concentration of mercury increased in brain up to 3 days, despite a declining mercury content in blood. The first-order rate of mercury uptake in brain was independent of the dose of methylmercury. In blood, methylmercury was largely confined to erythrocytes. Mercury concentrations in liver and kidney correlated with those in the blood. Mercuric chloride was distributed equally between erythrocytes and plasma in blood. Mice receiving mercuric chloride did not have appreciable levels of mercury in the brain throughout the sampling period. Coadministration of L-cysteine with mercuric chloride reduced mercury levels in the liver with no effect on brain concentrations. Glutathione depletion by diethylmaleate increased mercury concentration in brain after methylmercury treatment, whereas a decrease in kidney mercury concentration was observed. The results suggested that thiol compounds may not facilitate the entry of mercuric ion into the brain but can alter the distribution in other organs.

Differences in the uptake of cadmium and mercury by rat hepatocyte primary cultures: Role of a sulfhydryl carrier

Studies measuring the uptake of cadmium or mercury in isolated hepatocytes demonstrated that hepatocytes accumulated more cadmium than mercury in serum-containing medium, serum-free medium, or balanced salt solution. The preferential hepatocellular accumulation of cadmium, independent of medium composition, suggested that the uptake mechanism for cadmium and mercury might be different in hepatocytes. Pretreatment of hepatocytes with 50 μM N-ethylmaleimide decreased cadmium uptake by 23% while having no effect on the uptake of mercury uptake. Cadmium uptake in the presence of parachloromercuribenzenesulfonate or mercury was inhibited in a concentration-dependent manner. The uptake of cadmium was maximally inhibited (80%) with 75 μM parachloro-mercuribenzenesulfonate or 20 μM mercury respectively. Cadmium had no effect on mercury. Hepatocytes treated with parachloromercuribenzenesulfonate or mercury accumulated cadmium at a rate closely resembling the rate of mercury uptake in untreated hepatocytes. These results suggested that an SH-containing carrier may be operative in the uptake of cadmium by hepatocytes. Mercury can interact with this carrier to inhibit cadmium uptake; however, this carrier does appear to facilitate mercury uptake.

Role of catalase in the oxidation of mercury vapor

In human red blood cells the slow rate of production of hydrogen peroxide limits the rate of oxidation of mercury vapor. When H 2O 2 was added to blood samples, the rate of mercury uptake increased six times, but the inhibitory effect of KCN was less pronounced than in samples without H 2O 2, possibly because H 2O 2 tends to destroy cyanide. Only in the absence of exogenous H 2O 2 did the inhibition of oxidation of mercury vapor by different concentrations of KCN parallel the inhibition of catalase. Addition of peroxide to liver homogenates was without effect. When 20% (w/v) liver homogenates were exposed to mercury vapor at 37°, neither acatalasemia in mice nor pretreatment of rats with 2 g/kg of aminotriazole produced an appreciable decrease in the uptake of mercury during the 90-min incubation period. However, it was clear that catalase was responsible for the oxidation of mercury from the correlation ( r 2 = 0.85) between catalase activity and mercury uptake when 0.4 mg liver in 2 ml of incubation medium was exposed to mercury vapor. With higher concentrations of homogenates the availability of mercury limited the oxidation process. Experiments with horseradish peroxidase, beef liver catalase and inorganic catalysts of H 2O 2 decomposition indicate that the elemental mercury atom serves as an electron donor for complex I of catalase which is formed from the first reaction of catalase with H 2O 2. Other possible pathways of oxidation such as oxidation of elemental mercury by nascent oxygen released from H 2O 2 do not appear to be important.

Uptake of Mercury Vapor by Wheat

Using a whole-plant chamber and (203)Hg-labeled mercury, a quantitative study was made of the effect of environmental parameters on the uptake, by wheat (Triticum aestivum), of metallic mercury vapor, an atmospheric pollutant. Factors were examined in relation to their influence on components of the gas-assimilation model, [Formula: see text]where U(Hg) is the rate of mercury uptake per unit leaf surface, C(a)' is the ambient mercury vapor concentration, C(l)' is the mercury concentration at immobilization sites within the plant (assumed to be zero), r(l.Hg) is the total leaf resistance to mercury vapor exchange, and r(m.hg) is a residual term to account for unexplained physical and biochemical resistances to mercury vapor uptake.Essentially all mercury vapor uptake was confined to the leaves. r(l.hg) was particularly influenced by illumination (0 to 12.8 klux), but unaffected by ambient temperature (17 to 33 C) and mercury vapor concentration (0 to 40 mug m(-3)). The principal limitation to mercury vapor uptake was r(m.hg), which was linearly related to leaf temperature, but unaffected by mercury vapor concentration and illumination, except for apparent high values in darkness.Knowing C(a)' and estimating r(l.hg) and r(m.hg) from experimental data, mercury vapor uptake by wheat in light was accurately predicted for several durations of exposure using the above model.

Uptake of Mercury by Freshwater Clams (Family Unionidae)

Mercury concentrations were measured in water, sediments, and three species of clams from lakes with and without reported mercury contamination. Elevated mercury levels in clams were associated with elevated mercury levels in water and sediments.Uncontaminated clams were exposed to three mercury compounds at 1.0, 10, 50, and 100 μg Hg/liter for up to 3 wk in the laboratory. The clams concentrated the metal in the order methylmercuric chloride > phenylmercuric acetate > mercuric chloride. The rate of uptake of mercury increased with increasing mercury concentration in the water. In most cases, temperature had no effect on the rate of mercury uptake or elimination.The distribution among organs depended on the compound to which the clams had been exposed. Only methylmercuric chloride was concentrated extensively in foot muscle. Transfer of methylmercuric chloride among organs apparently continued after exposure to the compound had ended.