Volatilization of mercury from natural water by a broad-spectrum Hg-resistant Bacillus pasteurii strain DR2
TL;DR: A broad spectrum mercury-resistant bacterial strain was isolated from contaminated water and was identified as Bacillus pasteurii strain DR2 as mentioned in this paper, which could volatilize Hg-compounds including organomercurials from its growth media.
Abstract: A broad-spectrum mercury-resistant bacterial strain was isolated from contaminated water and was identified as Bacillus pasteurii strain DR2. It could volatilize Hg-compounds including organomercurials from its growth media. It utilized several aromatic compounds as a sole source of carbon. The bacterial strain eliminated HgCl2 from sterile river water and the presence of benzene, toluene, naphthalene and nitrobenzene at 1 mM concentration in the system increased the rate of mercury volatilization, the volatilization rate being highest with benzene. When 1.7×107 cells of this bacterial strain were added per ml of non-sterile water the bacterial strain volatilized more than 90 percent of mercury from mercuric chloride and organo-mercurials like PMA, thiomersol and methoxy ethyl mercuric chloride (MEMC). In the absence of this bacterial strain the volatilization of PMA and MEMC due to the presence of other Hg-resistant organisms in nonsterile polluted water ranged between 20–25 percent and of HgCl2 was about 40 percent. However, in the presence of B. pasteurii DR2 volatilization of these Hg-compounds from non-sterile water increased by 20–40 percent. In the presence of 1 mM benzene the rate of mercury volatilization was even higher. In all the cases the rate of volatilization was higher in the first seven days than in the next seven days.
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"Volatilization of mercury from natu..." refers background in this paper
...In many cases bacterial resistance to mercury compounds is plasmid mediated (Schottel et al., 1974; Silver and Misra, 1988 )....
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TL;DR: The mercury cycle in the biosphere and biological methylation of mercury and microbial resistance to mercury and organomercurials are studied.
Abstract: BIOTRANSFORMA nONS OF TOXIC MET AL CAnONS . Mercury . The mercury cycle in the biosphere .. Biological methylation of mercury . Microbial resistance to mercury and organomercurials .
413 citations
TL;DR: Much additional research is required before the relationship(s) between environmental pollution and neoplasms in indigenous aquatic species can be understood, and the current state of knowledge in the general areas of fish and shellfish metabolism and the use of aquatic animal models in studies of chemical carcinogenesis is described.
Abstract: This review of the literature on neoplastic or cancer-like disorders in fish and shellfish sets out to (1) summarize what is known of the occurrence of neoplastic diseases in indigenous populations of aquatic animals found in different geographic areas of the world; (2) critically evaluate existing reports so as to determine whether or not environmental pollutants are implicated as causal agents of the cellular disorders and (3) describe the current state of knowledge in the general areas of fish and shellfish metabolism and the use of aquatic animal models in studies of chemical carcinogenesis. Tumors and neoplasms have been described in fish and shellfish populations from many areas throughout the world. Although environmental pollutants have been suggested as the cause of neoplasms in at least some cases, the existing evidence does not permit a firm conclusion. For fish, the quality of the reports and data reviewed varied considerably. There are rather good experimental data to suggest that cancer-like conditions in fish from certain areas of Puget Sound (Washington), the Fox River (Illinois) and Japan are associated with chemical contaminants in the environment. The data purported to support a chemical etiology for highly publicized tumors in fish from the Buffalo River, Torch Lake and Black River are not of a high quality. Most of the studies from those areas are compromised by inadequate experimental designs, and further research will be necessary to achieve a more complete in relation to the existence of tumors in fish from those areas. There are also reports providing impressive evidence that chemical pollutants are not associated with neoplasms in fish, even in those inhibiting environments known to contain mutagenic substances. Large surveys conducted from highly polluted aquatic systems in Yugoslavia (Sava River), Germany (Rhine and Elbe Rivers) and Australia (Port Phillip Bay) all reported negative results. Many other studies and surveys have produced data that neither supported nor refuted a pollution-neoplasm association. In contrast to fish, there is little evidence that neoplasms of clams, oysters and mussels are associated in any significant way with environmental pollution. The most obvious conclusion, from reviewing the existing literature, is that much additional research is required before the relationship(s) between environmental pollution and neoplasms in indigenous aquatic species can be understood. There are severe constraints associated with conducting credible field studies in this area, given the incalculable number of variables in natural environments. In the future, it may be advisable to place more emphasis on laboratory studies employing state-of-the-art methods to provide fundamental information that can be used to understand the nature and causes of neoplasms in aquatic species.
191 citations
"Volatilization of mercury from natu..." refers background in this paper
...These compounds are often carcinogenic and enhance mutagenicity (Sato et al., 1983; Mix, 1986 )....
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...These compounds are mutagenic and teratogenic (Summers and Silver, 1978; Mix, 1986 )....
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TL;DR: THE AUTHORS have screened a large number of R plasmid-bearing Escherichia coli and obtained a few that confer resistance to the organomercurials phenylmercuric acetate (PMA) and methylmerCuric chloride (MMA), which are of interest to see if the mercury(ial) resistance of the bacteria in the alimentary canal influences the fate of ingested mercury(ials).
Abstract: WE have screened a large number of R plasmid-bearing Escherichia coli and obtained a few that confer resistance to the organomercurials phenylmercuric acetate (PMA) and methylmercuric chloride (MMA). Resistance to cationic Hg(II) in E. coli, Staphylococcus aureus and Pseudomonas aeruginosa has invariably been associated with plasmids that also mediate resistance to various antibiotics (R plasmids)1–6. The mechanism of mercury resistance, is the enzymatic reduction of Hg(II) to Hg(0), which is volatile2,7,8. Previously, no organomercurial-reducing E. coli strains have been reported. The only organomercurial-reducing strain studied in detail is a PMA-resistant soil pseu-domonad7–9. As organomercurials including PMA are a human health problem10, it will be of interest to see if the mercury(ial) resistance of the bacteria in our alimentary canal influences the fate of ingested mercury(ials).
175 citations
"Volatilization of mercury from natu..." refers background in this paper
...In many cases bacterial resistance to mercury compounds is plasmid mediated ( Schottel et al., 1974; Silver and Misra, 1988)....
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TL;DR: Except for very low hydrocarbon concentrations, the Monod model for a single substrate was able to describe reasonably well the time dependence of both cell growth and hydrocarbon consumption for experiments with n-decane.
Abstract: Batch experiments were conducted with a strain of Pseudomonas aeuroginsa and a strain of Ochrobactrum anthropi, both Gram-negative bacteria, growing on aqueous solutions containing straight-chain hydrocarbons solubilized in small micelles (204 nm) of nonionic surfactants. Measurements of optical density, a quantity proportional to bacterial cell concentration, and hydrocarbon content were made as a function of time. Since no macroscopic hydrocarbon drops were present and therefore there was no opportunity for the bacteria to attach themselves to oil-water interfaces, the results provided unambiguous confirmation that solubilization greatly enhances rates of hydrocarbon degradation in these systems compared to rates observed with bulk liquid hydrocarbon in the absence of surfactants. Solubilization of n-decane and n-tetradecane in micelles reduced the times required for cell density to double during exponential growth by a factor of {approximately}5 for one bacterial strain compared to results obtained for surfactant-free experiments. The improvement was even greater for the other strain. Except for very low hydrocarbon concentrations, the Monod model for a single substrate was able to describe reasonably well the time dependence of both cell growth and hydrocarbon consumption for experiments with n-decane. 28 refs., 4 figs.
143 citations