三峡库区消落带土壤中硫酸盐还原菌对汞甲基化作用的影响

为探究三峡水库这一特殊的周期性干湿交替环境中,硫酸盐还原菌(sulfate-reducing bacteria,SRB)是否在汞的生物甲基化过程中起主导作用,本文以库区消落带原土为研究对象,以灭菌土+接种硫酸盐还原菌Desulfovibrio africanus(D.africanus,DSM-2603)为对照(试验A),在每公斤土壤分别添加0、1、5 mg汞浓度条件下,模拟研究原土(试验B)中总汞(THg)和甲基汞(MeHg)含量的动态变化、总硫酸盐还原菌(SRB)数量变化,以及影响土壤中甲基汞含量的环境因子分析.结果表明,淹水状况有利于THg从土壤中释放,且Hg含量越高,释放越快;菌株D.africanus对汞具生态适应性,其菌数与MeHg含量显著正相关:在5 mg·kg~(-1)Hg条件下,D.africanus菌数可达3.65×10~4cfu·g~(-1),MeHg含量也高达7.60×10~4ng·kg~(-1).值得注意的是,试验B处理中,一方面消落区原土中SRB菌数较少,平均仅193 cfu·g~(-1);另一方面,土壤MeHg含量较低:在5mg·kg~(-1)Hg条件下,MeHg含量仅为5.54×10~3ng·kg~(-1),且总SRB菌数与MeHg含量无显著相关性.由此可以推测,在三峡水库消落区这种非严格厌氧土壤环境中,SRB并非优势菌群,其中还存在着其它对生物汞甲基化起主导作用的好氧或兼性厌氧微生物种群.     

Alkylation of metals and the activity of metal‐alkyls†

The biochemical basis for resistance to metal ion toxicity is emerging though it is complicated by the different resistance mechanisms. Several strategies for resistance to toxic metal ions have been identified:

1. The development of energy driven efflux pumps which keep toxic element levels low in the interior of the cell. Such mechanisms have been described for Cd(II) and As(V).

2. Oxidation (e.g. AsO^2‐ to AsO₄ ^3‐) or reduction (e.g. Hg²⁺ to Hg⁰) can enzymatically and intracellularly convert a more toxic form of an element to a less toxic form.

3. The biosynthesis of intracellular polymers which serve as traps for the removal of metal ions from solution such as traps have been described for cadmium, calcium, nickel and copper.

4. The binding of metal ions to cell surfaces.

5. The precipitation of insoluble metal complexes (e.g. metal sulfides and metal oxides) at cell surfaces.

6. Biomethylation and transport through cell‐membranes by diffusion controlled processes.

In this short review I shall discuss the implications of biomethylation as a detoxification mechanism for microorganisms as well as for certain higher organisms.     

A review of arsenicals in biology

The most toxic form of arsenic is arsine gas. Arsenite is also highly toxic and arsenate is moderately toxic. Arsine gas will lyse red blood cells, arsenite inactivates particular enzymes and arsenate uncouples oxidative phosphorylation. Arsenic does not appear to be a significant mutagen. Epidemiological studies have implicated arsenic as a cause of lung cancer and skin cancer, but arsenic generally does not induce cancer in laboratory animals. Arsenic may bioaccumulate in some plants and marine organisms. Bacteria can be resistant to arsenic by preventing arsenate from entering the cell (chromosomal resistance) or pumping arsenic out of the cell (plasmid resistance). Many different organisms, including mammals, have the ability to methylate inorganic arsenic. Biomethylation seems to be a mechanism of arsenic detoxification.     

Evaluation of initiation activity of dimethylarsinic acid: Initiation potential of rat hepatocarcinogenesis

There is a dearth of data on the initiation activity of dimethylarsinic acid (DMA (V)), a major metabolite of the ubiquitous environmental and occupational carcinogen and toxicant, arsenic (As). The initiation activity of DMA (V) was investigated on rat hepatocarcinogenesis with liver being a major target organ for As-induced carcinogenicity. A total of 50 rats at 10 weeks old were randomly divided in a nine-week medium-term bioassay into four groups. Groups 1 and 2 received 200 ppm of DMA (V) in drinking water for four weeks while groups 3 and 4 drank only tap water until the sixth week when groups 1 and 3 were given 0.01% 2-acetylaminofluorene (2-AAF) in their diet for two weeks in the promotion stage. All animals were subjected to two-third partial hepatectomy (PH) at the seventh week. Quantitative analysis of glutathione S-transferase placental form (GST-P) positive foci in liver, a pre-neoplastic marker of rat hepatocarcinogenesis, demonstrated higher numbers in group 1 (DMA (V) + 2-AAF) than 3 (2-AAF alone) at foci consisting of two–four cells and 15 or a greater number of cells. The numbers of GST-P positive foci consisting of five–nine cells were significantly higher in group 1 than 3. Foci consisting of 10–14 cells were also higher but not significantly different. The GST-P positive foci were apparently similar in groups 2 and 4. Expression of total GST-P positive foci was significantly higher in group 1 compared to 2, 3 or 4. The proliferating cell nuclear antigen (PCNA) test performed to clarify the apparent trend of GST-P data revealed significantly higher PCNA index in group 1. Data indicate weak initiation potential of DMA (V) and for the first time appear to provide evidence for initiation activity in DMA (V)-induced hepatocarcinogenesis in rats.