The natural chlorine cycle – fitting the scattered pieces

Chlorine is one of the most abundant elements on the surface of the earth. Until recently, it was widely believed that all chlorinated organic compounds were xenobiotic, that chlorine does not participate in biological processes and that it is present in the environment only as chloride. However, over the years, research has revealed that chlorine takes part in a complex biogeochemical cycle, that it is one of the major elements of soil organic matter and that the amount of naturally formed organic chlorine present in the environment can be counted in tons per km(2). Interestingly enough, some of the pieces of the chlorine puzzle have actually been known for decades, but the information has been scattered among a number of different disciplines with little or no exchange of information. The lack of communication appears to be due to the fact that the points of departure in the various fields have not corresponded; a number of paradoxes are actually revealed when the known pieces of the chlorine puzzle are fit together. It appears as if a number of generally agreed statements or tacit understandings have guided perceptions, and that these have obstructed the understanding of the chlorine-cycle as a whole. The present review enlightens four paradoxes that spring up when some persistent tacit understandings are viewed in the light of recent work as well as earlier findings in other areas. The paradoxes illuminated in this paper are that it is generally agreed that: (1) chlorinated organic compounds are xenobiotic even though more than 1,000 naturally produced chlorinated compounds have been identified; (2) only a few, rather specialised, organisms are able to convert chloride to organic chlorine even though it appears as if the ability among organisms to transform chloride to organic chlorine is more the rule than the exception; (3) all chlorinated organic compounds are persistent and toxic even though the vast majority of naturally produced organic chlorine is neither persistent nor toxic; (4) chlorine is mainly found in its ionic form in the environment even though organic chlorine is as abundant or even more abundant than chloride in soil. Furthermore, the contours of the terrestrial chlorine cycle are outlined and put in a concrete form by constructing a rough chlorine budget over a small forested catchment. Finally, possible ecological roles of the turnover of chlorine are discussed.     

Toxicity of organic and inorganic mercury species in differentiated human neurons and human astrocytes

Organic mercury (Hg) species exert their toxicity primarily in the central nervous system. The food relevant Hg species methylmercury (MeHg) has been frequently studied regarding its neurotoxic effects in vitro and in vivo. Neurotoxicity of thiomersal, which is used as a preservative in medical preparations, is to date less characterised. Due to dealkylation of organic Hg or oxidation of elemental Hg, inorganic Hg is present in the brain albeit these species are not able to readily cross the blood brain barrier. This study compared for the first time toxic effects of organic MeHg chloride (MeHgCl) and thiomersal as well as inorganic mercury chloride (HgCl₂) in differentiated human neurons (LUHMES) and human astrocytes (CCF-STTG1). The three Hg species differ in their degree and mechanism of toxicity in those two types of brain cells. Generally, neurons are more susceptible to Hg species induced cytotoxicity as compared to astrocytes. This might be due to the massive cellular mercury uptake in the differentiated neurons. The organic compounds exerted stronger cytotoxic effects as compared to inorganic HgCl₂. In contrast to HgCl₂ exposure, organic Hg compounds seem to induce the apoptotic cascade in neurons following low-level exposure. No indicators for apoptosis were identified for both inorganic and organic mercury species in astrocytes. Our studies clearly demonstrate species-specific toxic mechanisms. A mixed exposure towards all Hg species in the brain can be assumed. Thus, prospectively coexposure studies as well as cocultures of neurons and astrocytes could provide additional information in the investigation of Hg induced neurotoxicity.     

Operon mer: bacterial resistance to mercury and potential for bioremediation of contaminated environments

Mercury is present in the environment as a result of natural processes and from anthropogenic sources. The amount of mercury mobilized and released into the biosphere has increased since the beginning of the industrial age. Generally, mercury accumulates upwards through aquatic food chains, so that organisms at higher trophic levels have higher mercury concentrations. Some bacteria are able to resist heavy metal contamination through chemical transformation by reduction, oxidation, methylation and demethylation. One of the best understood biological systems for detoxifying organometallic or inorganic compounds involves the mer operon. The mer determinants, RTPCDAB, in these bacteria are often located in plasmids or transposons and can also be found in chromosomes. There are two classes of mercury resistance: narrow-spectrum specifies resistance to inorganic mercury, while broad-spectrum includes resistance to organomercurials, encoded by the gene merB. The regulatory gene merR is transcribed from a promoter that is divergently oriented from the promoter for the other mer genes. MerR regulates the expression of the structural genes of the operon in both a positive and a negative fashion. Resistance is due to Hg2+ being taken up into the cell and delivered to the NADPH-dependent flavoenzyme mercuric reductase, which catalyzes the two-electron reduction of Hg2+ to volatile, low-toxicity Hg0. The potential for bioremediation applications of the microbial mer operon has been long recognized; consequently, Escherichia coli and other wild and genetically engineered organisms for the bioremediation of Hg2+-contaminated environments have been assayed by several laboratories.     

Mercury toxicity in plants

Mercury poisoning has become a problem of current interest as a result of environmental pollution on a global scale. Natural emissions of mercury form two-thirds of the input; manmade releases form about one-third. Considerable amounts of mercury may be added to agricultural land with sludge, fertilizers, lime, and manures. The most important sources of contaminating agricultural soil have been the use of organic mercurials as a seed-coat dressing to prevent fungal diseases in seeds. In general, the effect of treatment on germination is favorable when recommended dosages are used. Injury to the seed increases in direct proportion to increasing rates of application. The availability of soil mercury to plants is low, and there is a tendency for mercury to accumulate in roots, indicating that the roots serve as a barrier to mercury uptake. Mercury concentration in aboveground parts of plants appears to depend largely on foliar uptake of Hg⁰ volatilized from the soil. Uptake of mercury has been found to be plant specific in bryophytes, lichens, wetland plants, woody plants, and crop plants. Factors affecting plant uptake include soil or sediment organic content, carbon exchange capacity, oxide and carbonate content, redox potential, formulation used, and total metal content. In general, mercury uptake in plants could be related to pollution level. With lower levels of mercury pollution, the amounts in crops are below the permissible levels. Aquatic plants have shown to be bioaccumulators of mercury. Mercury concentrations in the plants (stems and leaves) are always greater when the metal is introduced in organic form. In freshwater aquatic vascular plants, differences in uptake rate depend on the species of plant, seasonal growthrate changes, and the metal ion being absorbed. Some of the mercury emitted from the source into the atmosphere is absorbed by plant leaves and migrates to humus through fallen leaves. Mercury-vapor uptake by leaves of the C₃ speciesoats, barley, and wheat is five times greater than that by leaves of the C₄ species corn, sorghum, and crabgrass. Such differential uptake by C₃ and C₄ species is largely attributable to internal resistance to mercury-vapor binding. Airborne mercury thus seems to contribute significantly to the mercury content of crops and thereby to its intake by humans as food. Accumulation, toxicity response, and mercury distribution differ between plants exposed through shoots or through roots, even when internal mercury concentrations in the treated plants are similar. Throughfall and litterfall play a significant role in the cycling and deposition of mercury. The possible causal mechanisms of mercury toxicity are changes in the permeability of the cell membrane, reactions of sulphydryl (-SH) groups with cations, affinity for reacting with phosphate groups and active groups of ADP or ATP, and replacement of essential ions, mainly major cations. In general, inorganic forms are thought to be more available to plants than are organic ones. Plants can be exposed to mercurials either by direct administration as antifungal agents, mainly to crop plants through seed treatment or foliar spray, or by accident. The end points screened are seed germination, seedling growth, relative growth of roots and shoots, and, in some case, studies of leaf-area index, internode development, and other anatomical characters. Accidental exposures occur through soil, water, and air pollution. The level of toxicity is usually tested under laboratory conditions using a wide range of concentrations and different periods of exposure. Additional parameters include biochemical assays and genetical studies. The absorption of organic and inorganic mercury from soil by plants is low, and there is a barrier to mercury translocation from plant roots to tops. Thus, large increases in mercury levels in soil produce only modest increases in mercury levels in plants by direct uptake from soil. Injuries to cereal seeds caused by organic mercurials has been characterized by abnormal germination and hypertrophy of the roots and coleoptile. Mercury affects both light and dark reactions of photosynthesis. Substitution of the central atom of chlorophyll, magnesium, by mercury in vivo prevents photosynthetic light harvesting in the affected chlorophyll molecules, resulting in a breakdown of photosynthesis. The reaction varies with light intensity. A concentration and time-dependent protective effect of GSH seems to be mediated by the restricted uptake of the metal involving cytoplasmic protein synthesis. Plant cells contain aquaporins, proteins that facilitate the transport of water, in the vacuolar membrane (tonoplast) and the plasma membrane. Many aquaporins are mercury sensitive, and in AQP1 a mercury-sensitive cysteine residue (Cys-189) is present adjacent to a conserved Asn-Pro-Ala motif. At low concentrations mercury has a toxic effect on the degrading capabilities of microorganisms. Sensitivity to the metal can be enhanced by a reduction in pH, and tolerance of mercury by microorganisms has been found to be in the order: total population > nitrogen fixers > nitrifiers. Numerous experiments have been carried out to study the genetic effects of mercury compounds in experimental test systems using a variety of genetic endpoints. The most noticeable and consistent effect is the induction of c-mitosis through disturbance of the spindle activity, resulting in the formation of polyploid and aneuploid cells and c-tumors. Organomercurials have been reported to be 200 times more potent than inorganic mercury. Exposure to inorganic mercury reduces mitotic index in the root-tip cells and increases the frequency of chromosomal aberrations in degrees directly proportional to the concentrations used and to the duration of exposure. The period of recovery after removal of mercury is inversely related to the concentration and duration of exposure. Bacterial plasmids encode resistance systems for toxic metal ions, including Hg²⁺, functioning by energy-dependent efflux of toxic ions through ATPases and chemiosmotic cationproton antiporters. The inducible mercury resistance (mer) operon encodes both a mercuric ion uptake and detoxification enzymes. In gram-negative bacteria a periplasmic protein,MerP, an inner-membrane transport protein,MerT, and a cytoplasmic enzyme, mercuric reductase, theMerA protein, are responsible for the transport of mercuric ions into cells and their reduction to elemental mercury, Hg(II). InThiobacillus ferrooxidans, an acidophilic chemoautotrophic bacterium sensitive to mercury ions, a group of mercury-resistant strains, which volatilize mercury, has been isolated. The entire coding sequence of the mercury-ion resistance gene has been located in a 2.3 kb fragment of chromosomal DNA (encoding 56,000 and 16,000 molecular-weight proteins) from strain E-l 5 ofEscherichia coli. Higher plants andSchizosaccharomyces pombe respond to heavy-metal stress of mercury by synthesizing phytochelatins (PCs) that act as chelators. The strength of Hg(II) binding to glutathione and phytochelatins follows the order: γGlu-Cys-Gly(γGlu-Cys)₂Gly(γGlu-Cys)₃Gly(γGlu-Cys)₄Gly. Suspension cultures of haploid tobacco,Nicotiana tabacum, cells were subjected to ethyl methane sulfonate to raise mercury-tolerant plantlets. HgCl₂-tolerant variants were selected from nitrosoguanidine (NTG)-treated suspension cell cultures of cow pea,Vigna unguiculata, initiated from hypocotyl callus and incubated with 18 ⧎g/ml HgCl₂. Experiments have been carried out to develop mercury-tolerant plants ofHordeum vulgare through previous exposure to low doses of mercury and subsequent planting of the next generation in mercury-contaminated soil. Phytoremediation involves the use of plants to extract, detoxify, and/or sequester environmental pollutants from soil and water. Transgenic plants cleave mercury ions from methylmercury complexes, reduce mercury ions to the metallic form, take up metallic mercury through their roots, and evolve less toxic elemental mercury. Genetically engineered plants contain modified forms of bacterial genes that break down methyl mercury and reduce mercury ions. The first gene successfully inserted into plants wasmerA, which codes for a mercuric ion reductase enzyme, reducing ionic mercury to the less toxic elemental form.MerB codes for an organomercurial lyase protein that cleaves mercury ions from highly toxic methyl mercury compounds. Plants with themerB gene have been shown to detoxify methyl mercury in soil and water. Both genes have been successfully expressed inArabidopsis thaliana, Brassica (mustard),Nicotiana tabacum (tobacco), andLiriodendron tulipifera (tulip poplar). Plants currently being transformed include cattails, wild rice, andSpartina, another wetland plant. The problem of mercury contamination can be reduced appreciably by combining the standard methods of phytoremediation—removal of mercury from polluted areas through scavenger plants—with raising such plants both by routine mutagenesis and by genetic engineering. The different transgenics raised utilizing the two genesmerA andmerB are very hopeful prospects.     

Subcellular targeting of methylmercury lyase enhances its specific activity for organic mercury detoxification in plants

Methylmercury is an environmental pollutant that biomagnifies in the aquatic food chain with severe consequences for humans and other animals. In an effort to remove this toxin in situ, we have been engineering plants that express the bacterial mercury resistance enzymes organomercurial lyase MerB and mercuric ion reductase MerA. In vivo kinetics experiments suggest that the diffusion of hydrophobic organic mercury to MerB limits the rate of the coupled reaction with MerA (Bizily et al., 2000). To optimize reaction kinetics for organic mercury compounds, the merB gene was engineered to target MerB for accumulation in the endoplasmic reticulum and for secretion to the cell wall. Plants expressing the targeted MerB proteins and cytoplasmic MerA are highly resistant to organic mercury and degrade organic mercury at 10 to 70 times higher specific activity than plants with the cytoplasmically distributed wild-type MerB enzyme. MerB protein in endoplasmic reticulum-targeted plants appears to accumulate in large vesicular structures that can be visualized in immunolabeled plant cells. These results suggest that the toxic effects of organic mercury are focused in microenvironments of the secretory pathway, that these hydrophobic compartments provide more favorable reaction conditions for MerB activity, and that moderate increases in targeted MerB expression will lead to significant gains in detoxification. In summary, to maximize phytoremediation efficiency of hydrophobic pollutants in plants, it may be beneficial to target enzymes to specific subcellular environments.     

Comparative in vitro cytogenetic studies in mercury-exposed human lymphocytes

As part of a long-term cytogenetic research project on mercury, we studied the in vitro clastogenic capacity of HgCl2 and CH3HgCl as well as their influence on chromosome segregation by means of a computer-aided chromosome distribution study in metaphase plates. As in other in vitro studies published elsewhere, we exposed human peripheral blood lymphocytes to different concentrations of the mercury compound during a limited period of the pre-DNA synthetic stage (G1-S) or from that stage up to mitosis (G1-M). For both exposure periods and both mercury compounds we observed a rather important clastogenic effect as well as a dissociation of the (normally highly associated) acrocentrics. The results do indicate, in conjunction with previously published data, that mercury compounds alter the chromosome segregation at lower concentrations than those observed for clastogenicity. Moreover, the effects on chromosome segregation are not necessarily due to binding to spindle proteins. Binding to--and inactivation of RNA polymerase I may for example be another mechanism of action which is more important for the inorganic form of mercury than for the organic form.     

Studies on the mechanism of the stimulation of polymerase II-catalyzed RNA synthesis by mercury compounds

The specific stimulation of alpha-amanitin-sensitive RNA synthesis in isolated nuclei by methyl mercury (Frenkel, G. D., and Randles, K. (1982) J. Biol. Chem. 257, 6275-6279) has been further investigated. Using the method of alkaline hydrolysis/uridine analysis to determine the number of RNA chains growing in vitro, it was found that the stimulation could not be accounted for by an increase in the number of growing chains. The stimulatory effect of heparin (Coupar, B. E. H., and Chesterton, C. J. (1977) Eur. J. Biochem. 79, 525-533), was found to be additive with that of methyl mercury at saturating concentrations of the latter. Various detergents were found to affect RNA synthesis per se and to modify the stimulatory effect of methyl mercury, suggesting that the stimulation by methyl mercury requires a degree of structural integrity of some nuclear components. The ability of a number of other mercury compounds to stimulate RNA synthesis was investigated. None of the inorganic compounds examined, i.e. HgCl2, HgSO4, and Hg(ClO4)2, stimulated synthesis. Among the alkyl organic compounds tested in addition to methyl mercury, ethyl mercury also stimulated RNA synthesis, but dimethylmercury did not. Among the aryl compounds tested, phenylmercury did not stimulate synthesis whereas p-hydroxymercuribenzoate and p-hydroxymercuribenzenesulfonate did. N-Ethylmaleimide, a nonmercurous sulfhydryl reagent, was found to have only weak ability to stimulate RNA synthesis, compared to a comparable mercury-containing sulfhydryl reagent, p-hydroxymercuribenzoate. The stimulatory effect of the latter was, however, effectively competed out by the former, indicating that sulfhydryl binding is necessary for the stimulation but not sufficient. This conclusion was reinforced by experiments which utilized a model system to measure the ability of various mercury compounds to compete with N-ethylmaleimide in binding to cysteine. The results showed that even compounds such as phenylmercury and the inorganic mercurials, which are unable to stimulate RNA synthesis, are able to bind to a sulfhydryl group.     

Origin of organic compounds on the primitive earth and in meteorites

The role and relative contributions of different forms of energy to the synthesis of amino acids and other organic compounds on the primitive earth, in the parent bodies or carbonaceous chondrites, and in the solar nebula are examined. A single source of energy or a single process would not account for all the organic compounds synthesized in the solar system. Electric discharges appear to produce amino acids more efficiently than other sources of energy and the composition of the synthesized amino acids is qualitatively similar to those found in the Murchison meteorite. Ultraviolet light is also likely to have played a major role in prebiotic synthesis. Although the energy in the sun's spectrum that can be absorbed by the major constituents of the primitive atmosphere is not large, reactive trace components such as H2S and formaldehyde absorb at longer wavelengths where greater amounts of energy are available and produce amino acids by reactions involving hot hydrogen atoms. The thermal reaction of CO + H2 + NH3 on Fischer-Tropsch catalysts generates intermediates that lead to amino acids and other organic compounds that have been found in meteorites. However, this synthesis appears to be less efficient than electric discharges and to require a special set of reaction conditions. It should be emphasized that after the reactive organic intermediates are generated by the above processes, the subsequent reactions which produce the more complete biochemical compounds are low temperature homogenous reactions occurring in an aqueous environment.     

Polycyclic aromatic hydrocarbons: environmental pollution and bioremediation

Polycyclic aromatic hydrocarbons (PAHs) are widely distributed and relocated in the environment as a result of the incomplete combustion of organic matter. Many PAHs and their epoxides are highly toxic, mutagenic and/or carcinogenic to microorganisms as well as to higher systems including humans. Although various physicochemical methods have been used to remove these compounds from our environment, they have many limitations. Xenobiotic-degrading microorganisms have tremendous potential for bioremediation but new modifications are required to make such microorganisms effective and efficient in removing these compounds, which were once thought to be recalcitrant. Metabolic engineering might help to improve the efficiency of degradation of toxic compounds by microorganisms. However, efficiency of naturally occurring microorganisms for field bioremediation could be significantly improved by optimizing certain factors such as bioavailability, adsorption and mass transfer. Chemotaxis could also have an important role in enhancing biodegradation of pollutants. Here, we discuss the problems of PAH pollution and PAH degradation, and relevant bioremediation efforts.     

大米草对有机汞的耐性、吸收及转化

大米草对营养液中氯化甲基汞(MeHgCl)毒性的临界浓度为15 uml/L,是烟草的3倍.氯化甲基汞处理后,植株体内有机汞总量在增加,而营养液中有机汞总量在减少,无机汞总量则明显增加.这些结果表明,大米草可以吸收有机汞,将有机汞部分地转化为无机汞,并且无机汞较多地积累在植株的地下部,同时有一部分通过扩散或分泌进入营养液中.大米草对汞的积累作用和把有机汞转化为无机汞的转化作用在环境污染的植物修复方面有重要的利用价值.     

New insights into the metabolism of organomercury compounds: mercury-containing cysteine S-conjugates are substrates of human glutamine transaminase K and potent inactivators of cystathionine γ-lyase

Anthropogenic practices and recycling in the environment through natural processes result in release of potentially harmful levels of mercury into the biosphere. Mercury, especially organic forms, accumulates in the food chain. Mercury reacts readily with sulfur-containing compounds and often exists as a thiol S-conjugate, such as the l-cysteine (Cys)-S-conjugate of methylmercury (CH(3)Hg-S-Cys) or inorganic mercury (Cys-S-Hg-S-Cys). These S-conjugates are structurally similar to l-methionine and l-cystine/l-cystathionine, respectively. Bovine and rat glutamine transaminase K (GTK) catalyze transamination of sulfur-containing amino acids. Recombinant human GTK (rhGTK) has a relatively open catalytic active site, and we report here that this enzyme, like the rat and bovine enzymes, can also utilize sulfur-containing l-amino acids, including l-methionine, l-cystine, and l-cystathionine as substrates. The current study extends this list to include mercuric S-conjugates, and shows that CH(3)Hg-S-Cys and Cys-S-Hg-S-Cys are substrates and reversible inhibitors of rhGTK. The homocysteine S-conjugates, Hcy-S-Hg-S-Hcy and CH(3)Hg-S-Hcy, are also inhibitors. Finally, we show that HgCl(2), CH(3)Hg-S-Cys and Cys-S-Hg-S-Cys are potent irreversible inhibitors of rat cystathionine γ-lyase. The present study broadens our knowledge of the biochemistry of mercury compounds by showing that Cys S-conjugates of mercury interact with enzymes that catalyze transformations of biologically important sulfur-containing amino acids.     

Mercury as a risk factor for cardiovascular diseases

Mercury is a heavy metal that exists naturally in the environment. Major sources include the burning of fossil fuels (especially coal) and municipal waste incineration. Mercury can exist in several forms, with the most hazardous being organic methylmercury. In waterways (lakes, rivers, reservoirs, etc.), mercury is converted to methylmercury, which then accumulates in fish, especially in large predatory fish. Fish and fish products are the major--if not the only--source of methylmercury in humans. Mercury has long been recognized as a neurotoxin for humans, but in the last 10 years, its potentially harmful effects on cardiovascular diseases (CVD) have raised a cause for concern, mostly due to the proposed role of mercury in oxidative stress propagation. Some epidemiological studies have indeed found an association between increased levels of mercury in the body and risk of CVD. There are several plausible mechanisms to explain the association; these are discussed in this review. We also review the epidemiological studies that have investigated the association between mercury and CVD.     

Silver enhancement of tissue mercury: demonstration of mercury in autometallographic silver grains from rat kidneys

The autometallographic silver enhancement method has been applied increasingly to detect trace amounts of mercury in preparations of biological tissue. It has, however, been difficult to establish the presence of a core of mercury within the silver grain by direct methods such as energy dispersive X-ray analysis. In the present work, a sample of autometallographic silver grains was prepared from kidneys of rats exposed to mercury in the drinking water. Frozen sections from the kidneys were silver-enhanced and subsequently all organic material was removed by enzymatic digestion. The remaining pellet of silver grains was analyzed by proton-induced X-ray emission (PIXE) and mercury was demonstrated in an amount of 0.1-0.5% compared to silver. In addition, it was demonstrated that two pools of catalytic mercury compounds exist, probably corresponding to sulfide- and selenium-bound mercury.     

Volatilization of mercury by immobilized mercury-resistant bacterial cells

Highly toxic mercury compounds may come into the environment through the use of mercury compounds as disinfectants for hospital and household purposes, Hg catalyst in industries, burning of coal and petroleum products, mercury-based pesticides and fungicides used in agriculture, and seed dressings. Toxic effects of mercury can be counteracted by microbial cells through the enzymes mercuric reductase and organomercurial lyase. Immobilized mercury-resistant bacterial cells of Azotobacter chroococcum could effectively volatilize mercury from mercury-containing buffer and detoxify mercury compounds. Moreover, the efficiency of mercury volatilization was much greater than with the native cells, as immobilized cells can be reused. Immobilized cells continuously volatilized mercury from mercury-containing buffer after four consecutive 24 h cycles. The storage stability of immobilized cells was much better than that of the native cells.     

Prebiotic phosphate: a problem insoluble in water ? ]

It is well-known that in water phosphate readily reacts with calcium, precipitating as insoluble apatite. How phosphorus could have been available for prebiotic reactions is still an open problem. We suggest that phosphorus-containing compounds might have accumulated in a hydrophobic medium, since the absence of calcium ions would have prevented them from precipitating as apatite. Hydrophobic compounds may have been synthesized on the early Earth through the polymerization of methane or through Fischer-Tropsch-type reactions. Moreover, hydrophobic compounds would have been delivered to the early Earth by extraterrestrial infall. In previous articles (Morchio and Traverso [1999], Morchio et al. [2001]) we suggested that such hydrophobic material would have formed a hydrophobic layer on the surface of the sea, which would have provided an environment thermodynamically more suitable than water for the concentration and polymerization of organic molecules fundamental to life, particularly amino acids and (pyrimidine) bases. It may be hypothesized that elemental phosphorus or phosphorus-containing compounds (such as phosphite) deriving from volcanic eruptions would have ended up raining down into the hydrophobic layer, accumulating due to the absence of calcium ions, in an environment protected against hydrolysis. Phosphorus-containing compounds might have interacted with hydrophobic molecules in the layer giving rise to polymers. In particular, phosphite might have reacted with the hydrophobic amino acids, giving rise to phosphoamino acids, which, in turn, might have interacted with pyrimidine bases (relatively abundant in the layer) giving rise to peptides and oligonucleotide-like polymers. Indeed, it has been experimentally shown (Zhou et al. [1996]) that, in an anhydrous organic medium (pyridine), dialkilphosphite reacts with amino acids to form phosphoamino acids, which interact with pyrimidine nucleosides to give nucleotides, short oligonucleotides and phosphoryl peptides.     

Genotoxicity of mercury compounds. A review

This article reviews literature data concerning the genotoxicity of 29 mercury-containing agents, including laboratory compounds as well as ingredients of preparations used as fungicides, dyes, disinfectants and drugs. A variety of genetic end-points were investigated in bacteria, yeasts, moulds, plants, insects, cultured cells from fishes, rodents or humans, aquatic organisms, amphibians, mammalia and exposed humans. The overall evaluation is quite complex. Mercury compounds failed to induce point mutations in bacteria but often exerted clastogenic effects in eukaryotes, especially by binding SH groups and acting as spindle inhibitors, thereby causing c-mitosis and consequently aneuploidy and/or polyploidy. Inorganic mercury compounds were also found to induce the generation of reactive oxygen species and glutathione depletion in cultured mammalian cells. Although different mercury compounds tended to produce qualitatively comparable genetic effects, which suggests the involvement of a common toxic entity, methylmercury derivatives and other ionizable organomercury compounds were more active in short-term tests than either non-ionizable mercury compounds (e.g., dimethylmercury) or inorganic mercury salts (e.g., mercuric chloride). The results of cytogenetic monitoring in peripheral blood lymphocytes of individuals exposed to elemental mercury or mercury compounds from accidental, occupational or alimentary sources were either negative or borderline or uncertain as to the actual role played by mercury in some positive findings. Both genotoxic and non-genotoxic mechanisms may contribute to the renal carcinogenicity of mercury, which so far has been convincingly demonstrated only in male rodents treated with methylmercury chloride.     

Microbial transformations of tin and tin compounds

Summary The use of organotins for agricultural and industrial purposes and in the marine environment has been increasing steadily for more than 20 years. Recently, reliable methodologies have been developed to permit quantification of individual molecular species of organotins in cultures and in the environment. Particular attention has been given to methyltins which can be formed abiotically and by microorganisms, and to tributyltins which are toxic components of effective antifouling paints. In the aquatic environment tin, tributyltins and other organotins accumulate in the surface microlayer, in sediments, and on suspended particulates. Tin compounds are toxic to a variety of organisms and some aquatic organisms can bioaccumulate them. When tin compounds, particularly di-or tri-substituted tins, enter an ecosystem, a portion of the microbial population is killed. Among the survivors are organisms which can methylate inorganic or organic tins, but the relative contribution of biotic and abiotic mechanisms is not clear. While many details of methylations and demethylations need to be worked out, it is clear that transformations of tins can influence the toxicity, volatility and mobility of tin in natural ecosystems. Tributyltins can be debutylated by microorganisms, and hydroxybutyl tins may be intermediates, as they are in mammalian systems. Little is known of the potential and probable microbial transformations of other economically important organotins, but the transformations should be studied for they may have industrial and environmental importance.