汞在新建水库食物网中生物累积与风险评价研究进展

汞是唯一参与全球循环的液态重金属。1974年,自美国学者Smith首次报道水库中鱼类总汞含量高于邻近自然湖泊以来,水库中鱼类汞升高的风险成为新建水库环境影响评价中的重要内容之一。汞在水库生态系统生物组分和非生物组分中含量升高的现象先后在世界各国报道,包括加拿大、美国、芬兰、泰国和巴西等。通过对系列的野外研究进行回顾,表明了水库形成后生态系统中汞的甲基化过程发生了变化。水库形成对汞在食物网中的鱼类、底栖生物、浮游生物的累积产生影响。水库中汞的生物累积、迁移转化主要与被淹没土壤和植物腐解过程有着直接或间接的关系。水库形成后,总汞、甲基汞和甲基汞比例在生态系统食物网各组分中的变化并不一致。蓄水后,水体中总汞变化较小,甲基汞和甲基汞比例上升明显;浮游生物尤其是浮游动物中总汞升高,但甲基汞和甲基汞比例升高更为明显;与浮游动物类似,底栖水生昆虫中总汞升高,甲基汞和甲基汞比例升高也更为明显;鱼类作为食物网顶级消费者,甲基汞比例一般在80%以上,在水库形成后鱼类总汞和甲基汞均明显升高,但甲基汞比例变化已经不大。这些变化揭示了水库形成后甲基汞在食物网传递的两个主要可能途径,一是微型生物食物网。通过悬浮颗粒物、浮游植物、浮游动物这一环节,甲基汞和甲基汞比例有明显的增加。第二个途径是底层生物食物网。通过悬浮颗粒物、细菌、碎屑食性底栖水生昆虫、肉食型底栖水生昆虫环节,甲基汞和甲基汞比例明显增加。这两种途径均能导致以水生昆虫、小鱼、甲壳类等为食的肉食性鱼类汞含量增加。水库形成后,生态系统中汞的甲基化发生了明显的"加速"过程。这种"加速"过程最直接的因素是成库后大量土壤淹没使得汞的甲基化平衡被打破。这个过程主要有两方面的影响。一方面是直接影响,被淹没土壤和植被在腐解过程中主动或被动地将甲基汞释放到水库生态系统中;另一方面是间接影响,被淹没土壤和植被的腐解使水库底部形成厌氧环境,有利于无机汞从被淹没土壤和植被中溶出,为甲基化反应提供充裕的、可供甲基化的无机汞,同时腐解产生的大量营养物质为微生物提供丰富食物来源,使硫酸盐还原菌大量繁殖,促进无机汞的甲基化。在我国,有关汞在新建水库食物网中生物累积和风险评价的研究有待进一步加强。     

Mercury methylation independent of the acetyl-coenzyme A pathway in sulfate-reducing bacteria

Sulfate-reducing bacteria (SRB) in anoxic waters and sediments are the major producers of methylmercury in aquatic systems. Although a considerable amount of work has addressed the environmental factors that control methylmercury formation and the conditions that control bioavailability of inorganic mercury to SRB, little work has been undertaken analyzing the biochemical mechanism of methylmercury production. The acetyl-coenzyme A (CoA) pathway has been implicated as being key to mercury methylation in one SRB strain, Desulfovibrio desulfuricans LS, but this result has not been extended to other SRB species. To probe whether the acetyl-CoA pathway is the controlling biochemical process for methylmercury production in SRB, five incomplete-oxidizing SRB strains and two Desulfobacter strains that do not use the acetyl-CoA pathway for major carbon metabolism were assayed for methylmercury formation and acetyl-CoA pathway enzyme activities. Three of the SRB strains were also incubated with chloroform to inhibit the acetyl-CoA pathway. So far, all species that have been found to have acetyl-CoA activity are complete oxidizers that require the acetyl-CoA pathway for basic metabolism, as well as methylate mercury. Chloroform inhibits Hg methylation in these species either by blocking the methylating enzyme or by indirect effects on metabolism and growth. However, we have identified four incomplete-oxidizing strains that clearly do not utilize the acetyl-CoA pathway either for metabolism or mercury methylation (as confirmed by the absence of chloroform inhibition). Hg methylation is thus independent of the acetyl-CoA pathway and may not require vitamin B(12) in some and perhaps many incomplete-oxidizing SRB strains.     

The effect of aqueous speciation and cellular ligand binding on the biotransformation and bioavailability of methylmercury in mercury-resistant bacteria

Mercury resistant bacteria play a critical role in mercury biogeochemical cycling in that they convert methylmercury (MeHg) and inorganic mercury to elemental mercury, Hg(0). To date there are very few studies on the effects of speciation and bioavailability of MeHg in these organisms, and even fewer studies on the role that binding to cellular ligands plays on MeHg uptake. The objective of this study was to investigate the effects of thiol complexation on the uptake of MeHg by measuring the intracellular demethylation-reduction (transformation) of MeHg to Hg(0) in Hg-resistant bacteria. Short-term intracellular transformation of MeHg was quantified by monitoring the loss of volatile Hg(0) generated during incubations of bacteria containing the complete mer operon (including genes from putative mercury transporters) exposed to MeHg in minimal media compared to negative controls with non-mer or heat-killed cells. The results indicate that the complexes MeHgOH, MeHg-cysteine, and MeHg-glutathione are all bioavailable in these bacteria, and without the mer operon there is very little biological degradation of MeHg. In both Pseudomonas stutzeri and Escherichia coli, there was a pool of MeHg that was not transformed to elemental Hg(0), which was likely rendered unavailable to Mer enzymes by non-specific binding to cellular ligands. Since the rates of MeHg accumulation and transformation varied more between the two species of bacteria examined than among MeHg complexes, microbial bioavailability, and therefore microbial demethylation, of MeHg in aquatic systems likely depends more on the species of microorganism than on the types and relative concentrations of thiols or other MeHg ligands present.     

Mercury Methylation Independent of the Acetyl-Coenzyme A Pathway in Sulfate-Reducing Bacteria

Sulfate-reducing bacteria (SRB) in anoxic waters and sediments are the major producers of methylmercury in aquatic systems. Although a considerable amount of work has addressed the environmental factors that control methylmercury formation and the conditions that control bioavailability of inorganic mercury to SRB, little work has been undertaken analyzing the biochemical mechanism of methylmercury production. The acetyl-coenzyme A (CoA) pathway has been implicated as being key to mercury methylation in one SRB strain, Desulfovibrio desulfuricans LS, but this result has not been extended to other SRB species. To probe whether the acetyl-CoA pathway is the controlling biochemical process for methylmercury production in SRB, five incomplete-oxidizing SRB strains and two Desulfobacter strains that do not use the acetyl-CoA pathway for major carbon metabolism were assayed for methylmercury formation and acetyl-CoA pathway enzyme activities. Three of the SRB strains were also incubated with chloroform to inhibit the acetyl-CoA pathway. So far, all species that have been found to have acetyl-CoA activity are complete oxidizers that require the acetyl-CoA pathway for basic metabolism, as well as methylate mercury. Chloroform inhibits Hg methylation in these species either by blocking the methylating enzyme or by indirect effects on metabolism and growth. However, we have identified four incomplete-oxidizing strains that clearly do not utilize the acetyl-CoA pathway either for metabolism or mercury methylation (as confirmed by the absence of chloroform inhibition). Hg methylation is thus independent of the acetyl-CoA pathway and may not require vitamin B₁₂ in some and perhaps many incomplete-oxidizing SRB strains.     

Accumulation of mercury in estuarine food chains

To understand the accumulation of inorganic mercury and methylmercury at the base of the estuarine food chain, phytoplankton (Thalassiosira weissflogii) uptake and mercury speciation experiments were conducted. Complexation of methylmercury as methylmercury-bisulfide decreased the phytoplankton uptake rate while the uptake rate of the methylmercury-cysteine and -thiourea complexes increased with increasing complexation by these ligands. Furthermore, our results indicated that while different ligands influenced inorganic mercury/methylmercury uptake by phytoplankton cells, the ligand complex had no major influence on either where the mercury was sequestered within the phytoplankton cell nor the assimilation efficiency of the mercury by copepods. The assimilation efficiency of inorganic mercury/methylmercury by copepods and amphipods feeding on algal cells was compared and both organisms assimilated methylmercury much more efficiently; the relative assimilation efficiency of methylmercury to inorganic mercury was 2.0 for copepods and 2.8 for amphipods. The relative assimilation is somewhat concentration dependent as experiments showed that as exposure concentration increased, a greater percentage of methylmercury was found in the cytoplasm of phytoplankton cells, resulting in a higher concentration in the copepods feeding on these cells. Additionally, food quality influenced assimilation by invertebrates. During decay of a T. weissflogii culture, which served as food for the invertebrates, copepods were increasingly less able to assimilate the methylmercury from the food, while even at advanced stages of decay, amphipods were able to assimilate mercury from their food to a high degree. Finally, fish feeding on copepods assimilated methylmercury more efficiently than inorganic mercury owing to the larger fraction of methylmercury found in the soft tissues of the copepods.     

Degradation of Methylmercury by Bacteria Isolated from Environmental Samples

A total of 207 bacterial cultures, isolated from environmental samples, was screened for ability to degrade methylmercury. Of these, 30 were found positive for aerobic demethylation. Twenty-two of these were shown to be facultative anaerobes and 21 of these degraded methylmercury anaerobically. All positive species volatilized methylmercury aerobically, and methane was produced as a degradation product. Although methylmercury degradation was complete in most cases, material balances indicated some of the inorganic mercury formed was not volatilized and is presumed bound to the cells. All positive isolates were tolerant to at least 0.5 mug of methylmercury per ml, and the extent of volatilization of mercury increased with concentration to the threshold value. The results indicate that demethylating species are prevalent in the environment and may be important in suppressing the methylmercury content of sediments.     

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.     

Effect of subchronic administration of ethanol and methylmercury in combination on the tissue distribution of mercury in rats

The effect of oral administration for 14 weeks of 8 g.kg-1.day-1 ethanol and 0.5 mg.kg-1.day-1 methylmercuric chloride in combination to rats fed isocaloric diets has been investigated. Ethanol, in contrast to published studies, failed to influence the tissue distribution of methylmercury and its inorganic mercury metabolite in brain and kidney, and did not inhibit the increase in kidney weight induced by methylmercury. Ethanol and methylmercury, in combination and individually, reduced the renal but not the hepatic activity of gamma-glutamyltransferase, but did not affect the renal and biliary concentration of reduced glutathione. Further study is required to determine the circumstances under which ethanol can influence the tissue distribution of methylmercury and its inorganic mercury metabolite.     

COMPARATIVE EFFECTS OF ORGANIC AND INORGANIC MERCURY ON BRAIN SLICE RESPIRATION AND METABOLISM

—Respiration and carbohydrate metabolism were measured in guinea-pig brain slices exposed to organic and inorganic mercury. Organic mercury decreased oxygen uptake and ¹⁴CO₂ production at consistently lower concentrations than inorganic mercury. Organic mercury also caused a striking elevation of pyruvate and lactate at low doses where inorganic mercury had no effect on respiration or metabolism. A unique inhibition of tricarboxylic acid cycle function is suggested and might partially explain the distinctive neurotoxicity of organic mercury.     

Methylmercury distribution, metabolism, and neurotoxicity in the mouse brain

Methylmercury distribution, biotransformation, and neurotoxicity in the brain of male Swiss albino mice were investigated. Mice were orally dosed with [203 Hg]methylmercury chloride (10 mg/kg) for 1 to 9 days. Methylmercury was evenly distributed among the posterior cerebral cortex, subcortex, brain stem, and cerebellum. The The anterior cerebral cortex had a significantly higher methylmercury concentration than the rest of the brain. The distribution of methylmercury's inorganic mercury metabolite was found to be uneven in the brain. The pattern of distribution was cerebellum greater than brain stem greater than subcortex greater than cerebral cortex. The order of the severity of histological damage was cerebral cortex greater than cerebellum greater than subcortex greater than brain stem. There was no correlation between methylmercury distribution in the brain and structural brain damage. However, there was a relationship between the distribution of methylmercury's inorganic mercury metabolite and structural damage in the anterior cerebral cortex (positive correlation) and the anterior subcortex (negative correlation). There was also a positive correlation between the fraction of methylmercury's metabolite of the total mercury present and structural brain damage in the anterior cerebral cortex. This study suggests that biotransformation may have a role in mediating methylmercury neurotoxicity.     

The chemical forms of mercury and selenium in whale skeletal muscle

Human exposure to potentially neurotoxic methylmercury species is a public-health concern for many populations worldwide. Both fish and whale are known to contain varying amounts of methylmercury species. However studies of populations that consume large quantities of fish or whale have provided no clear consensus as to the extent of the risk. The toxicological profile of an element depends strongly on its chemical form. We have used X-ray absorption spectroscopy to investigate the comparative chemical forms of mercury and selenium in fish and whale skeletal muscle. The predominant chemical form of mercury in whale is found to closely resemble that found in fish. In the samples of skeletal muscle studied, no involvement of selenium in coordination of mercury is indicated in either whale or fish, with no significant inorganic HgSe or HgS type phases being detected. The selenium speciation in fish and whale shows that similar chemical types are present in each, but in significantly different proportions. Our results suggest that for equal amounts of Hg in skeletal muscle, the direct detrimental effects arising from the mercury content from consuming skeletal muscle from whale and fish should be similar if the effects of interactions with other components in the meat are not considered.     

Experimental study of the bioaccumulation of inorganic mercury and methylmercury in the goldfish (Carassius auratus L.)

The study of the mercury and methylmercury bioaccumulation by various species of fish is only possible experimentally when the animals are maintained fasting during a few days. With a such experimentation in the goldfish (Carassius auratus L.), the authors are showing that methylmercury is much more accumulated than inorganic mercury: the transfert factor is about 760 to 780 for the methylmercury chloride and only 90 for the mercuric chloride. In fact a lot of variables occur in this phenomena of bioaccumulation (experimentation time, size and age of fish, solvant space, concentration of oxygen and mercury in water,...) and make this study difficult.     

Determination of Mercury and Methylmercury in Hair of the Czech Children’s Population

The developed method for mercury speciation analysis has been validated and used for the biomonitoring study of mercury species in human hair. Statistical evaluation proved the reliability of simplified determination of inorganic mercury (difference between total mercury and methylmercury). The results of the validation showed that the method is very well suitable for the determination of both species of mercury in hair for biomonitoring purposes. Non-exposed schoolchildren from three areas in the western and central part of the Czech Republic were chosen as the target group. Tenth of a microgram per gram of the total mercury were generally found in the analyzed hair; values higher than 1 μg g⁻¹ were detected only exceptionally. Comparable results were obtained for two western areas and differed significantly from those for the third area located in the central part of the Czech Republic. In the areas examined, the mean methylmercury contents amounted to 23–46% of the total mercury in the hair. The results confirm an assumption that exposure to mercury does not pose a significant risk to the population in the Czech Republic.     

蓟运河汉沽地区河泥中汞的微生物甲基化作用

汞的生物转化作用的研究开始于60年代末,Wood等(1968)研究了生物甲基化的机制,认为汞甲基化有酶和非酶两种作用,甲基化作用是通过甲基钴氨素中的甲基转移来完成的。瑞典生物学家Jensen和Jernel(?)v(1969)提出在湖泊底泥里微生物有形成甲基汞的功能,汞甲基化的速度与底泥里的微生物活动有密切的相关性。由此,微生物汞甲基化作用得到人们的注视,Yamada等(1972)在厌氧条件下研究了匙形梭菌(Clostridium cochlearium)的汞甲基化作用。Vonk等(1973)发现在通气条件下一些细菌和真菌可使氯化汞甲基化形成少量的甲基汞。Fagerstr(?)m和Jernel(?)v(1972)曾报道,通气条件下汞转化过程中甲基化的主要产物是一甲基汞,厌氧条件下汞甲基化的产物大部是二甲基汞。但是,人们总是认为甲基化的主要产物为一甲基汞,而二甲基汞形成的数量则很少(Iverson等,1978)。这些汞化合物在水体中引起危害。     

Mercury Reduces Avian Reproductive Success and Imposes Selection: An Experimental Study with Adult- or Lifetime-Exposure in Zebra Finch

Mercury is a global pollutant that biomagnifies in food webs, placing wildlife at risk of reduced reproductive fitness and survival. Songbirds are the most diverse branch of the avian evolutionary tree; many are suffering persistent and serious population declines and we know that songbirds are frequently exposed to mercury pollution. Our objective was to determine the effects of environmentally relevant doses of mercury on reproductive success of songbirds exposed throughout their lives or only as adults. The two modes of exposure simulated philopatric species versus dispersive species, and are particularly relevant because of the heightened mercury-sensitivity of developing nervous systems. We performed a dosing study with dietary methylmercury in a model songbird species, the zebra finch (Taeniopygia guttata), at doses from 0.3 – 2.4 parts per million. Birds were exposed to mercury either as adults only or throughout their lives. All doses of mercury reduced reproductive success, with the lowest dose reducing the number of independent offspring produced in one year by 16% and the highest dose, representing approximately half the lethal dose for this species, causing a 50% reduction. While mercury did not affect clutch size or survivorship, it had the most consistent effect on the proportion of chicks that fledged from the nest, regardless of mode of exposure. Among birds exposed as adults, mercury caused a steep increase in the latency to re-nest after loss of a clutch. Birds exposed for their entire lifetimes, which were necessarily the offspring of dosed parents, had up to 50% lower reproductive success than adult-exposed birds at low doses of methylmercury, but increased reproductive success at high doses, suggesting selection for mercury tolerance at the highest level of exposure. Our results indicate that mercury levels in prey items at contaminated sites pose a significant threat to populations of songbirds through reduced reproductive success.     

A comparative study of the toxicity of mercury dichloride and methylmercury, assayed by the Frog Embryo Teratogenesis Assay--Xenopus (FETAX)

The Frog Embryo Teratogenesis Assay-Xenopus (FETAX) is a powerful and flexible bioassay that makes use of the embryos of the anuran amphibian Xenopus laevis. The FETAX can detect xenobiotics that affect embryonic development, when mortality, teratogenicity and growth inhibition are used as endpoints. The FETAX was used to compare the embryotoxic and teratogenic potentials of two chemical species of mercury, inorganic mercury(II) chloride (HgCl2) and organic methylmercury chloride (MeHgCl). A higher toxicity of MeHgCl (the estimated median lethal concentration [LC50] and median teratogenic concentration [TC50] were 0.313microM and 0.236microM, respectively) over HgCl2, with estimated LC50 and TC50 values of 0.601microM and 0.513microM, respectively). On the basis of these results, HgCl2 and MeHgCl can be classified as "slightly teratogenic compounds", as the ratio of LC50/TC50 is less than 1.5. There was a significant deviation from the commonly described monotonic behaviour of the concentration-response curves, suggesting a hormetic effect of both species of mercury. Uptake experiments, followed by neutron activation analysis, showed a higher incorporation of mercury in embryos exposed to MeHgCl compared with those exposed to HgCl2. Interestingly, Hg- exposed embryos showed a higher content of selenium and zinc than did control embryos.     

Sediment Microbial Community Composition and Methylmercury Pollution at Four Mercury Mine–Impacted Sites

Mercury pollution presents a globally significant threat to human and ecosystem health. An important transformation in the mercury cycle is the conversion of inorganic mercury to methylmercury, a toxic substance that negatively affects neurological function and bioaccumulates in food chains. This transformation is primarily bacterially mediated, and sulfate-reducing bacteria (SRB) have been specifically implicated as key mercury methylators in lake and estuarine sediments. This study used phospholipid fatty acid (PLFA) analysis to investigate sediment microbial community composition at four abandoned mercury mine–impacted sites in the California Coast Range: the Abbott, Reed, Sulphur Bank, and Mt. Diablo mines. Differences in watershed and hydrology among these sites were related to differences in microbial community composition. The Abbott and Sulphur Bank mines had the highest levels of methylmercury. Floc (a type of precipitate that forms when acid mine drainage contacts lake or river water) and sediment samples differed in terms of several important environmental variables and microbial community composition, but did not have statistically different methylmercury concentrations. Quantification of PLFA biomarkers for SRB (10Mel6:0 for Desulfobacter and i17:1 for Desulfovibrio) revealed that Desulfobacter and Desulfovibrio organisms made up higher percentages of overall microbial biomass at the Sulphur Bank and Mt. Diablo mines than at the Abbott and Reed mines. Correlations between these SRB biomarker fatty acids and methylmercury concentrations suggest that Desulfobacter and Desulfovibrio organisms may contribute to methylmercury production in the Abbott, Reed, and Sulphur Bank mines but may not be important contributors to methylmercury in the Mt. Diablo Mine.     

Effects of complexing agents on the distribution of Hg(II) species provided by food to starfish Leptasterias polaris

Abstract

Mature starfish Leptasterias polaris were exposed to labelled mercury (II) species via food contaminated at a level of 5.0 μg g^?1. The distribution of inorganic Hg and methylmercury (MeHg) in starfish organs and tissues and the effect of a series of complexing agents on mercury translocation between organs and tissues were examined over a 24-h period. The distribution of mercury species in coelomic fluid components, ammonia excretion rate and mercury excretion were also measured. The highest concentrations were observed in the stomach (the source organ) and in pyloric caecum (up to 0.32 μg g^?1 wet weight for inorganic Hg and 0.22 μg g^?1 for MeHg). Concentrations of MeHg in gonads ranged from ≤ 0.01 to 0.08 μg g^?1 whereas concentrations of inorganic Hg never exceeded 0.06 μg g^?1. In all studied cases, mercury concentration was very low the coelomic fluid (≤ 0.01 μg g^?1). The short-term distribution of Hg species via contaminated food in starfish L. polaris seems to be controlled by the haemal system, a primitive circulatory system responsible for the transport of soluble nutrients from the digestive track towards organs and tissues, but a possible role of the coelomic fluid can not be excluded. Very low Hg contents were observed in gonads and in the coelomic fluid which fills the general cavity. Except for mercaptoethanol (merOH) and dimercaptosuccinic acid (DMSA), the addition of complexing agents to the food had little effect on the distribution of Hg species. MerOH appeared as an efficient carrier for methylmercury transport through the digestive system. DMSA enhanced the translocation of inorganic mercury from stomach and pyloric caecum toward external tissues and markedly increased its excretion.     

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.     

Degradation of methylmercury by selenium

When methylmercury was incubated in the presence of selenite and reduced glutathione (GSH), the mercury which was extracted into benzene under acidic condition decreased gradually with the elapse of time. This decrease was due to the cleavage of mercury-carbon bond of methylmercury. The reaction did not proceed when selenite or GSH was singly added to the reaction mixture. L-Cysteine, 2-mercaptoethanol and sodium sulfide in place of GSH also were effective for decomposition of methylmercury in combination with selenite, but oxidized glutathione (GSSG) and L-cystine were not. This suggests that reduction of selenite is needed for the degradation of methylmercury. Thus, the effect of reduced metabolites of selenite produced by GSH was investigated. Glutathione selenotrisulfide (GSSeSG) requierd GSH for the degradation of methylmercury, whereas H₂Se possessed a strong activity even in the absence of GSH. This may indicate that H₂Se is involved directly in the conversion of methylmercury to inorganic mercury. This phenomenon found in $\text{in vitro}$ experiments is discussed in relation to the biotransformation of methylmercury.