汞污染对水稻土微生物和酶活性的影响

通过盆栽试验,研究了两种水稻土中不同汞处理的微生物学和酶学效应.结果表明：水稻收获后,除部分土壤的呼吸强度和代谢商随汞处理浓度的增加而持续增加外,不同浓度汞处理后土壤微生物量碳、呼吸强度、土壤脲酶、酸性磷酸酶和脱氢酶均表现为在低浓度汞处理(<2 mg Hg·kg^-1)时升高,而在高浓度汞处理(≥2 mg Hg·kg^-1)时则下降.土壤微生物商是对汞处理比较敏感的微生物学指标.黄红壤不同浓度汞处理的土壤酶活性大于小粉土.对重金属生态剂量ED₅₀进行分析表明,汞对小粉土脲酶活性和黄红壤磷酸酶活性的生态毒性均较强.     

汞化合物对红细胞膜作用的研究

本文研究了汞化合物对红细胞膜作用的光谱变化,观察了膜蛋白的荧光和磷光,膜上DPH的荧光偏振和ANS与红细胞膜的结合,以及他们与汞产生红血球溶血的关系。 在5P7.5缓冲液中红细胞膜蛋白的荧光随HgCl_2 Hg(AC)_2和PCMB的浓度加大而降低,表现为快和慢双相变化的过程,其淬灭作用的大小为HgCl_2>Hg(AC)_2PCMB,这是由于膜上形成了不发荧光的R—Trp—Hg~ 络合物以及能量从Trp转移到R—S—Hg~ 络合物上。HgCl_2对膜蛋白磷光的作用也是随汞离子浓度加大而降低,但磷光/荧光比则是增加的。标记红细胞膜的DPH偏振度是随HgCl_2浓度增加,表明膜流动性是随汞离子浓度加大而降低。标记膜上的ANS的荧光强度随HgCl_2和Hg(AC)_2的浓度加大而增加,这是由于ANS与膜的结合数随汞离子浓度加大而增加的缘故。上述各种变化是与汞离子对红血球溶血的作用一致的。     

利用丝状绿藻处理含汞污水的试验

用刚毛藻科的丝状绿藻为材料,进行了藻类处理含汞(HgCl2)污水的试验。Hg++浓度为0.5,1.0,2.0,5.0和10.0毫克/升,鲜藻与污水的重量之比为1∶100,4小时内,汞的去除率为70%。进行了藻类连续去汞能力的测定,10克鲜藻依次放入4个含汞污水的水样中(水量均为1升,Hg++浓度平均为3.61毫克/升),在每个水样停留时间为6小时,结果汞的去除率分别为76.8,78.4,61.8,53.1%,平均为67.5%,藻类含汞浓度以鲜重计算达到970ppm。利用藻类四级串联处理含汞量为4.0毫克/升的污水,停留时间共计24小时,总去除率达94%。从试验结果看来,藻类对汞的去除,主要是借助于表面吸附与细胞积累作用,与藻类的光合作用无关。但是0.1—10毫克/升的汞,都明显地抑制藻类的光合放氧,这种抑制作用在藻类接触汞4小时以后表现出来。       

利用丝状绿藻处理含汞污水的试验

用刚毛藻科的丝状绿藻为材料,进行了藻类处理含汞(HgCl2)污水的试验。Hg 浓度为0．5,1．0,2．0,5．0和10．0毫克／升,鲜藻与污水的重量之比为1：100,4小时内,汞的去除率为70％。进行了藻类连续去汞能力的测定,10克鲜藻依次放入4个含汞污水的水样中(水量均为1升,Hg 浓度平均为3．61毫克／升),在每个水样停留时间为6小时,结果汞的去除率分别为76．8,78．4,61．8,53．1％,平均为67．5％,藻类含汞浓度以鲜重计算达到970ppm。、利用藻类四级串联处理含汞量为4．0毫克／升的污水,停留时间共计24小时,总去除率达94％。从试验结果看来,藻类对汞的去除,主要是借助于表面吸附与细胞积累作用,与藻类的光合作用无关。但是0．1—10毫克／升的汞,都明显地抑制藻类的光合放氧,这种抑制作用在藻类接触汞4小时以后表现出来。     

问题解答

问:高中课本第9页中说:“糖类的分子式可以用通式C_n(H_2O)_m来表示(n和m可以相同,也可以不同)”请将n和m相同与不同的举例说明。答:糖类化合物是指具有多羟基醛或多羟基酮结构的一大类化合物。糖由碳、氢、氧三种元素组成。其中氢和氧的比例为2:1,就象氢和氧在水分子中的比例一样。所以糖的通式可写成C_n(H_2O)_m,并因此被称为碳水化合物。如赤藓糖的分子式为C_4H_8O_4,可写成C_4(H_2O)_4;核糖的分子式为C_5H_(10)O_5,可写成C_5(H_2O)_5;葡萄糖的分子式为C_6H_(12)O_6,可写成C_6(H_2O)_6等。     

呲啶的汞化及醋酸亚汞的制备

在人体内若干汞化合物能杀灭一些寄生虫及细菌,但其毒性较高,其中二价汞的毒性远高于一价汞化合物,有机汞化合物由于较难离解成汞离子而毒性也因之较低。鱼类的寄生虫或细菌是否可以用汞化合物抑制,是否有兴趣的。鱼病治疗中不必如治疗人类疾病时要用到静脉或肌肉注射,汞化合物毒性的顾虑可能也因之较少。     

贵州盘县煤矸石中汞的环境效应

通过冷原子荧光方法测定了贵州盘县新鲜煤矸石、不同风化程度煤矸石及煤矸石风化土壤中植物的Hg含量,对该地煤矸石中汞的分布规律及其环境效应进行了研究。结果表明,新鲜煤矸石中汞含量平均为(0.137±0.076) μg·g^-1,未表现异常富集。不同风化程度的煤矸石土壤Hg含量未有明显的变化规律,平均含量为(0.154±0.056) μg·g^-1,略高于土壤背景值。但在自燃后的煤矸石风化土壤和受其淋滤影响的下部土壤中汞却表现为异常富集,平均含量高达(1.627±0.294) μg·g^-1。煤矸石风化土壤尤其是自燃后的煤矸石风化土壤中Hg的植物可利用性都比较高,部分农作物中Hg含量超过了国家标准中食品Hg含量限值,要选择合适的作物进行栽培。     

吡啶的汞化及醋酸亚汞的制备

在人体内若干汞化合物能杀灭一些寄生虫及细菌,但其毒性较高,其中二价汞的毒性远高于一价汞化合物,有机汞化合物由于较难离解成汞离子而毒性也因之较低。鱼类的寄生虫或细菌是否可以用汞化合物抑制,是饶有兴趣的。鱼病治疗中不必如治疗人类疾病时要用到静脉或肌肉注射。汞化合物毒性的顾虑可能也因之较少。醋酸β-呲啶汞(β-Pyridylmercuric acetate)(Ia)治疗鱼病的作用会有国外文献报导。呲啶的汞化甚是不易,1923年Sachs及Ebertartinger首先试验,以后McClelland及Wilson将呲啶在高温用醋酸汞汞化,Swaney等将此法的作用条件进行了系统研究,找到在少量水存在及高压下加热至155℃,产率可达49％,并且可避免进一步汞化而形     

生物炭与氮肥对旱作春玉米农田CO_2和CH_4排放特征的影响

为了研究生物炭与氮肥对旱作春玉米农田CO_2和CH_4排放通量季节变化、累积排放总量及CO_2+CH_4排放强度的影响,试验设置C_0N_0(不加生物炭,不施氮肥)、C_0N_1(不加生物炭,施氮肥225kg·hm~(-2))和C_1N_1(添加生物炭50t·hm~(-2),施氮肥225kg·hm~(-2))3个处理,采用密闭式静态暗箱-气相色谱法对不同生物炭和氮肥输入旱作春玉米农田CO_2和CH_4排放通量进行连续观测,同时对影响通量变化的0~20cm土层温度和水分因子进行测定。结果表明:(1)试验期内不同处理春玉米农田均表现为CO_2累积通量的源,且CO_2排放通量均呈现一定的峰值变化规律。(2)C_1N_1处理减少了春玉米生长季农田CO_2排放通量和累积排放总量,在试验的2个生长季内农田CO_2平均排放通量和累积排放总量各处理均表现为C_0N_0C_0N_1C_1N_1,且C_1N_1处理降低显著。(3)土壤CO_2排放通量与土壤温度变化呈显著正相关关系,可用指数方程和二次方程较好拟合二者关系,且与10cm土层温度的相关性优于0cm土层温度,但土壤CO_2排放通量与土壤含水量呈负相关关系。(4)试验各处理农田土壤CH_4排放通量在-16.08~-73.96μg·m~(-2)·h~(-1)之间,表现为大气CH_4的净吸收库;C_1N_1处理增加了土壤CH_4排放通量和累积排放总量,但作用效果的显著性受年际环境因子的影响;农田土壤CH_4排放通量与土壤含水量呈显著正相关关系,与土壤温度呈显著负相关关系。研究发现,添加生物炭和施氮减少了旱作农田春玉米生长季CO_2排放通量和累积排放总量,增加了CH_4排放通量和累积排放总量,总体上显著增加了春玉米产量,显著减少农田CO_2+CH_4排放强度。     

汞对慈姑活性氧代谢和染色体的影响

研究了不同浓度Hg2 以及处理时间对慈姑叶和根的活性氧(reactive oxygen species,ROS)和染色体的影响。结果显示：汞能诱导慈姑叶和根大量产生ROS,其中H2O2的突发早于O2。0．5-5mg／L处理组染色体畸变率(Chromosomal aberrant frequency,CAF)和微核率(micronucleus frequency,MCNF)在72h内与处理浓度、时间呈正相关。CAF、MCNF所反映的细胞遗传毒性的大小主要取决于汞处理浓度,而ROS则起次要作用。H2O2很可能在慈姑抵御汞胁迫中起信号传导作用;慈姑通过促进根部部分细胞死亡提高抗汞能力。     

13C magnetic resonance investigation of mercury (II) binding to nucleosides and thiolated nucleosides in dimethyl sulfoxide.

Natural abundance, proton-decoupled 13C magnetic resonance spectroscopy is shown to be a useful technique for identifying the mercury (II) binding sites on nucleosides and especially thiolated nucleosides. Measurements made on dimethyl sulfoxide-d6 solutions, 0.5 M in nucleoside and 0.15 M in mercury, reveal that both CH3 HgCl and HgCl2 bind principally to the sulfur atoms of s6 Guo and s8 Guo. The 13C NMR spectra of the unthiolated nucleosides in the presence of excess (4:1) mercury reveal that HgCl2 binds to N-3 of cytidine, to more than one site on adenosine and guanosine, but not strongly to uridine. Excess HgCl2 shifts the thiocarbonyl carbon atoms in s6 Guo and s8 Guo approx. 16 ppm upfield compared to the free nucleosides, and there is evidence for additional coordination to N-7 of s6 Guo. Binding to the ribose hydroxyl groups is clearly ruled out. At least in these instances, 13C NMR proves to be useful for assigning the mercury (II) binding sites, complementing the results of proton magnetic resonance studies. Proton NMR data for the binding of CH3 HgCl and HgCl2 to s6 Guo and s8 Guo are also presented.     

Effects of dissolved organic carbon and salinity on bioavailability of mercury.

Hypotheses that dissolved organic carbon (DOC) and electrochemical charge affect the rate of methylmercury [CH3Hg(I)] synthesis by modulating the availability of ionic mercury [Hg(II)] to bacteria were tested by using a mer-lux bioindicator (O. Selifonova, R. Burlage, and T. Barkay, Appl. Environ. Microbiol. 59:3083-3090, 1993). A decline in Hg(II)-dependent light production was observed in the presence of increasing concentrations of DOC, and this decline was more pronounced at pH 7 than at pH 5, suggesting that DOC is a factor controlling the bioavailability of Hg(II). A thermodynamic model (MINTEQA2) was used to select assay conditions that clearly distinguished among various Hg(II) species. By using this approach, it was shown that negatively charged forms of mercuric chloride (HgCl3-/HgCl(4)2-) induced less light production than the electrochemically neutral form (HgCl2), and no difference was observed between the two neutral forms, HgCl2 and Hg(OH)2. These results suggest that the negative charge of Hg(II) species reduces their availability to bacteria and may be one reason why accumulation of CH3Hg(I) is more often reported to occur in freshwater than in estuarine and marine biota.     

A methylene blue-mediated enzyme electrode for the determination of trace mercury(II), mercury(I), methylmercury, and mercury-glutathione complex

A methylene blue-mediated enzyme biosensor has been developed for the detection of inhibitors including mercury(II), mercury(I), methylmercury, and mercury-glutathione complex. The inhibition to horseradish peroxidase was apparently reversible and noncompetitive in the presence of HgCl2 in less than 8 s and irreversibly inactivated when incubated with different concentrations of HgCl2 for 1-8 min. The binding site of horseradish peroxidase with HgCl2 probably was a cysteine residue SH. Mercury compounds can be assayed amperometrically with the detection limits 0.1 ng ml(-1) Hg for HgCl2 and methylmercury, 0.2 ng ml(-1) Hg for Hg2(NO3)2 and 1.7 ng ml(-1) Hg for mercury glutathione complex. Inactivation of the immobilized horseradish peroxidase was displayed in the AFM images of the enzyme membranes.     

Methylation and demethylation of mercury under controlled redox, pH and salinity conditions.

In estuarine sediments, the microbially mediated processes of methylation, demethylation, and volatilization determine the state and overall toxicity of mercury pollutants. The effects of redox potential (Eh) and salinity on the above microbial processes were investigated in reactors constructed to allow for continuous monitoring and adjustment of the pH (6.8) and Eh of freshly collected estuarine sediments. For measurements of methylation and demethylation activity, sediment slurries adjusted to appropriate salinity were spiked with HgCl2 or CH3HgCl, respectively, and were incubated in the reactors. Methylmercury was measured by gas chromatography. Volatilized elemental mercury (Hg0) was trapped and determined by cold vapor atomic absorption spectrometry. Volatilization of Hg0 and CH3HgCH3 were found to be minimal. Methylation of Hg2+ was favored at Eh-220 mV as compared to +110 mV. At -220 mV, high salinity (2.5%) inhibited methylation, and low salinity (0.4%) favored it. At +110 mV, the salinity effect was less pronounced. Demethylation of CH3HgCl was favored at +110 mV regardless of the salinity level. Low redox potential under low salinity conditions inhibited demethylation, but high salinity reversed this inhibition. These findings are helpful for interpreting and predicting the behavior of mercury pollutants in estuarine sediments.     

Effects of methyl mercury, mercuric sulfide and cinnabar on active avoidance responses, Na+/K+-ATPase activities and tissue mercury contents in rats

This study compared the neurobehavioral toxicities of three mercurial compounds: methyl mercury (MeHg) which is soluble and organic. and mercuric sulfide (HgS) and cinnabar (naturally occurring HgS), which are insoluble and inorganic. Cinnabar, a Chinese mineral medicine, is still used as a sedative in some Asian countries, but there is relatively little toxicological information about it. These mercurial compounds were administered intraperitoneally (MeHg, 2 mg/ kg) or orally (HgS and cinnabar, 1.0 g/kg) to male rats once every day for 13 consecutive days with assays conducted during or after discontinuous administration for 1 h, 2, 8 and 33 weeks. Neurotoxicity was assessed based on the active avoid-ance response and locomotor activity. The results obtained showed that MeHg and cinnabar prominently and irreversibly caused a decrease in body weight, prolongation of latency for escape from electric shock, a decrease in the percentage for the conditioned avoidance response (CAR) to electric shock, impairment of spontaneous locomotion and inhibition of Na+/K+-ATPase activity of the cerebral cortex. In contrast. HgS reversibly inhibited spontaneous locomotion and Na+/K+-ATPase activity. It was noted that HgS significantly decreased the latency of escape from electric shock during the ad-ministration period, which lasted for 33 weeks after discontinuous administration. In fact that pretreatment with arecoline (a cholinergic receptor agonist) but not fipexide (a dopaminergic receptor agonist) could significantly shorten the prolonged latency for escape caused by MeHg and cinnabar, suggested that the deficit in the active avoidance response was perhaps, at least in part, mediated by the dysfunction of the cholinergic rather than the dopaminergic system. Determination of the Hg levels of the whole blood and cerebral cortex revealed that the tissue mercury content was highly correlated with the degree of neurobehavioral toxicity of these Hg compounds. These findings suggest that insoluble HgS and cinnabar can be absorbed from the G-I tract and distributed to the brain. The possibility that contamination due to other minerals in the cinnabar is responsible for the greater neurotoxic effects compared to HgS is under investigation.     

Inhibition of the human thioredoxin system. A molecular mechanism of mercury toxicity

Mercury toxicity mediated by different forms of mercury is a major health problem; however, the molecular mechanisms underlying toxicity remain elusive. We analyzed the effects of mercuric chloride (HgCl(2)) and monomethylmercury (MeHg) on the proteins of the mammalian thioredoxin system, thioredoxin reductase (TrxR) and thioredoxin (Trx), and of the glutaredoxin system, glutathione reductase (GR) and glutaredoxin (Grx). HgCl(2) and MeHg inhibited recombinant rat TrxR with IC(50) values of 7.2 and 19.7 nm, respectively. Fully reduced human Trx1 bound mercury and lost all five free thiols and activity after incubation with HgCl(2) or MeHg, but only HgCl(2) generated dimers. Mass spectra analysis demonstrated binding of 2.5 mol of Hg(2+) and 5 mol of MeHg(+)/mol of Trx1 with the very strong Hg(2+) complexes involving active site and structural disulfides. Inhibition of both TrxR and Trx activity was observed in HeLa and HEK 293 cells treated with HgCl(2) or MeHg. GR was inhibited by HgCl(2) and MeHg in vitro, but no decrease in GR activity was detected in cell extracts treated with mercurials. Human Grx1 showed similar reactivity as Trx1 with both mercurial compounds, with the loss of all free thiols and Grx dimerization in the presence of HgCl(2), but no inhibition of Grx activity was observed in lysates of HeLa cells exposed to mercury. Overall, mercury inhibition was selective toward the thioredoxin system. In particular, the remarkable potency of the mercury compounds to bind to the selenol-thiol in the active site of TrxR should be a major molecular mechanism of mercury toxicity.     

In vitro setting of dose-effect relationships of 32 metal compounds in the Balb/3T3 cell line, as a basis for predicting their carcinogenic potential

The results are reported of the second stage in a programme for a systematic in vitro study on the carcinogenic potential of metal compounds with Balb/3T3 clone A31-1-1 mouse fibroblasts. Nineteen metal compounds that exhibited a strong cytotoxic effect during a previous screening run with a 100 microM fixed dose were tested with a 72-hour exposure over a wide range of concentrations (from 0.1 microM to 1000 microM), to produce dose-effect curves to permit extrapolation of the 50% inhibition concentration (IC50) values for each metal compound. This allows the establishment of a suitable range of doses for individual metal species, for use in the subsequent Balb/3T3 assay based on a two-stage concurrent cytotoxicity and morphological transformation protocol. Another 13 metal compounds were also tested, to determine whether the Balb/3T3 cell transformation assay is really a valuable in vitro model in relation to the problem of metal speciation. Of the metal compounds assayed, 26 showed a dose related cytotoxic response with calculated IC50 values ranging from 0.25 microM (CH3HgCl) to 140 microM [(C5H5)2TiCl2], whereas six metal compounds, namely (NH4)6Mo7O24*4H2O, CH3AsO(OH)2, C2H6AsNaO2(3H2O, KBr, CrCl3*6H2O and (NH4)2[TiO(C2O4)2]*H2O, displayed no observable cytotoxicity or low cytotoxicity at all the doses tested. The determination of IC50 values permits a ranking of the cytotoxicity responses of metal compounds with the highest cytotoxicities. Dose-effect curves and IC50 values of different chemical forms of individual metal compounds of As, Br, Cr, Hg, Ir, Pt, Te, Ti and V (cationic/anionic inorganic or organometallic species) showed clearly how the chemical nature of the metal strongly influences the toxic response. This confirms that the Balb/3T3 cell line is a valuable in vitro model with respect to the problem of metal speciation. This is a fundamental aspect to be considered when incorporating the results from in vitro cell transformation assays of the carcinogenic potential of metal compounds into regulatory testing schemes. In this context, the choice of test metal species for the development and validation of such assays cannot disregard the possibility that humans will be exposed to specific chemical forms of individual metal compounds (different oxidation states, and inorganic or organometallic natures) that can profoundly affect their toxicity.     

Biotoxicity of mercury as influenced by mercury(II) speciation

Integration of physicochemical procedures for studying mercury(II) speciation with microbiological procedures for studying the effects of mercury on bacterial growth allows evaluation of ionic factors (e.g., pH and ligand species and concentration) which affect biotoxicity. A Pseudomonas fluorescens strain capable of methylating inorganic Hg(II) was isolated from sediment samples collected at Buffalo Pound Lake in Saskatchewan, Canada. The effect of pH and ligand species on the toxic response (i.e., 50% inhibitory concentration [IC50]) of the P. fluorescens isolated to mercury were determined and related to the aqueous speciation of Hg(II). It was determined that the toxicities of different mercury salts were influenced by the nature of the co-ion. At a given pH level, mercuric acetate and mercuric nitrate yielded essentially the same IC50s; mercuric chloride, on the other hand, always produced lower IC50s. For each Hg salt, toxicity was greatest at pH 6.0 and decreased significantly (P = 0.05) at pH 7.0. Increasing the pH to 8.0 had no effect on the toxicity of mercuric acetate or mercuric nitrate but significantly (P = 0.05) reduced the toxicity of mercuric chloride. The aqueous speciation of Hg(II) in the synthetic growth medium M-IIY (a minimal salts medium amended to contain 0.1% yeast extract and 0.1% glycerol) was calculated by using the computer program GEOCHEM-PC with a modified data base. Results of the speciation calculations indicated that complexes of Hg(II) with histidine [Hg(H-HIS)HIS+ and Hg(H-HIS)2(2+)], chloride (HgCl+, HgCl2(0), HgClOH0, and HgCl3-), phosphate (HgHPO4(0), ammonia (HgNH3(2+), glycine [Hg(GLY)+], alanine [Hg(ALA)+], and hydroxyl ion (HgOH+) were the Hg species primarily responsible for toxicity in the M-IIY medium. The toxicity of mercuric nitrate at pH 8.0 was unaffected by the addition of citrate, enhanced by the addition of chloride, and reduced by the addition of cysteine. In the chloride-amended system, HgCl+, HgCl2(0), and HgClOH0 were the species primarily responsible for observed increases in toxicity. In the cysteine-amended system, formation of Hg(CYS)2(2-) was responsible for detoxification effects that were observed. The formation of Hg-citrate complexes was insignificant and had no effect on Hg toxicity.     

Differential mercury volatilization by tobacco organs expressing a modified bacterial merA gene

INTRODUCTIONEnvironmental pollution is an increasing prob-lem both fOr developing and developed countries.Mercury, both in organic and ionic fOrm, is one of themost hazardous pollutants among the heavy met-als[l]and its accumuIation in human body results ininactivation of metabolic enzymes and structuralproteins[2, 3] giving rise to serious health problems(Minamatasyndrome).Usually mercury pollution is caused by indus-trial and agricultural activities, releasing mercuryinto air, water an…     

Biotoxicity of mercury as influenced by mercury(II) speciation.

Integration of physicochemical procedures for studying mercury(II) speciation with microbiological procedures for studying the effects of mercury on bacterial growth allows evaluation of ionic factors (e.g., pH and ligand species and concentration) which affect biotoxicity. A Pseudomonas fluorescens strain capable of methylating inorganic Hg(II) was isolated from sediment samples collected at Buffalo Pound Lake in Saskatchewan, Canada. The effect of pH and ligand species on the toxic response (i.e., 50% inhibitory concentration [IC50]) of the P. fluorescens isolated to mercury were determined and related to the aqueous speciation of Hg(II). It was determined that the toxicities of different mercury salts were influenced by the nature of the co-ion. At a given pH level, mercuric acetate and mercuric nitrate yielded essentially the same IC50s; mercuric chloride, on the other hand, always produced lower IC50s. For each Hg salt, toxicity was greatest at pH 6.0 and decreased significantly (P = 0.05) at pH 7.0. Increasing the pH to 8.0 had no effect on the toxicity of mercuric acetate or mercuric nitrate but significantly (P = 0.05) reduced the toxicity of mercuric chloride. The aqueous speciation of Hg(II) in the synthetic growth medium M-IIY (a minimal salts medium amended to contain 0.1% yeast extract and 0.1% glycerol) was calculated by using the computer program GEOCHEM-PC with a modified data base. Results of the speciation calculations indicated that complexes of Hg(II) with histidine [Hg(H-HIS)HIS+ and Hg(H-HIS)2(2+)], chloride (HgCl+, HgCl2(0), HgClOH0, and HgCl3-), phosphate (HgHPO4(0), ammonia (HgNH3(2+), glycine [Hg(GLY)+], alanine [Hg(ALA)+], and hydroxyl ion (HgOH+) were the Hg species primarily responsible for toxicity in the M-IIY medium. The toxicity of mercuric nitrate at pH 8.0 was unaffected by the addition of citrate, enhanced by the addition of chloride, and reduced by the addition of cysteine. In the chloride-amended system, HgCl+, HgCl2(0), and HgClOH0 were the species primarily responsible for observed increases in toxicity. In the cysteine-amended system, formation of Hg(CYS)2(2-) was responsible for detoxification effects that were observed. The formation of Hg-citrate complexes was insignificant and had no effect on Hg toxicity.