Arsenic metabolism in cyanobacteria

Environmental context Cyanobacteria are ecologically important, photosynthetic organisms that are widely distributed throughout the environment. They play a central role in arsenic transformations in terms of both mineralisation and formation of organoarsenic species as the primary producers in aquatic ecosystems. In this review, arsenic resistance, transport and biotransformation in cyanobacteria are reviewed and compared with those in other organisms. Abstract Arsenic is a toxic element that is widely distributed in the lithosphere, hydrosphere and biosphere. Some species of cyanobacteria can grow in high concentrations of arsenate (pentavalent inorganic arsenic compound) (100mM) and in low-millimolar concentrations of arsenite (trivalent inorganic arsenic compound). Arsenate, which is a molecular analogue of phosphate, is taken up by cells through phosphate transporters, and inhibits oxidative phosphorylation and photophosphorylation. Arsenite, which enters the cell through a concentration gradient, shows higher toxicity than arsenate by binding to sulfhydryl groups and impairing the functions of many proteins. Detoxification mechanisms for arsenic in cyanobacterial cells include efflux of intracellular inorganic arsenic compounds, and biosynthesis of methylarsonic acid and dimethylarsinic acid through methylation of intracellular inorganic arsenic compounds. In some cyanobacteria, ars genes coding for an arsenate reductase (arsC), a membrane-bound protein involved in arsenic efflux (arsB) and an arsenite S-adenosylmethionine methyltransferase (arsM) have been found. Furthermore, cyanobacteria can produce more complex arsenic species such as arsenosugars. In this review, arsenic metabolism in cyanobacteria is reviewed, compared with that in other organisms. Knowledge gaps remain regarding both arsenic transport (e.g. uptake of methylated arsenicals and excretion of arsenate) and biotransformation (especially production of lipid-soluble arsenicals). Further studies in these areas are required, not only for a better understanding of the role of cyanobacteria in the circulation of arsenic in aquatic environments, but also for their application to arsenic bioremediation.

Iron antagonism of MSMA herbicide applied to bermudagrass: characterization of the Fe2+-MAA complexation reaction

Discoloration of bermudagrass often results from application of MSMA herbicide used to control southern crabgrass and other weeds. However, when products containing iron sulfate (FeSO4) are tank-mixed with MSMA, this discoloration is reduced. Experiments investigated the effect of tank-mixing organic arsenical herbicides with FeSO4or a chelated iron source (Sprint 330) in terms of southern crabgrass control and injury to bermudagrass. Tank-mixing MSMA with FeSO4reduced bermudagrass injury. However, southern crabgrass control was also reduced by at least 50% with the addition of ≥0.38 kg Fe2+ha−1. Neither antagonism nor safening of bermudagrass was observed when the chelated Fe2+source was used. Applying FeSO4as a separate treatment 1 to 4 d before or after MSMA application did not reduce visual burmudagrass injury 1 wk after treatment. Solution pH and FeSO4concentration controlled the extent of complexation and level of antagonism observed in the field; inorganic Fe2+reacted with MSMA to form a complex having reduced herbicidal activity. Potentiometric and spectrophotometric investigations found that methylarsonate, the parent acid of MSMA and other organic arsenical herbicides, reacts with inorganic Fe2+to form a stable 1:1 Fe2+-methylarsonic acid chelate having two points of metal coordination and a stability constant log10(β) = 2.77 ± 0.04. Tank-mixing MSMA with FeSO4to protect against bermudagrass injury negates the benefit of applying the herbicide for weed control, and therefore is not a recommendable practice for turf managers.

The response of tomato (Lycopersicon esculentum) to different concentrations of inorganic and organic compounds of arsenic

Tomato plants were cultivated in greenhouse and water solutions of arsenite (As(III)), arsenate (As(V)), methylarsonic acid (MA) and dimethylarsinic acid (DMA) were applied individually into cultivation substrate at two As levels, 5 and 15 mg kg−1 of the substrate. Comparing the availability of arsenic compounds increased in order arsenite = arsenate < MA < DMA where the arsenic contents in plants decreased during vegetation period. Within a single plant, the highest arsenic concentration was found in roots followed in decreasing order by leaves, stems, and fruits regardless of arsenic compound applied. Arsenic toxicity symptoms reflected in suppressed growth of plants and a lower number and size of fruits were most significant with DMA treatment. However, the highest accumulation of arsenic by plants growing in the soil containing DMA was caused by higher mobility of this compound in the soil due to its lower sorption affinity. Our results confirmed substantial role of transformation processes of arsenic compounds in soil in uptake and accumulation of arsenic by plants.

Weed Management in Cotton with CGA-362622, Fluometuron, and Pyrithiobac

An experiment was conducted at five locations in North Carolina during 2000 and 2001 to evaluate weed control, crop injury, and cotton yield. Weed management systems included different combinations of pyrithiobac preemergence (PRE), fluometuron PRE, CGA-362622 postemergence (POST), pyrithiobac POST, and monosodium salt of methylarsonic acid (MSMA) plus prometryn applied late POST-directed (LAYBY). At Goldsboro in 2000, cotton was injured 74 to 78% by CGA-362622 POST when evaluated 4 to 7 d after treatment (DAT). Injury at Clayton, Goldsboro, and Lewiston in 2001 and Rocky Mount in 2000 was less than 16% 4 to 7 DAT with the same treatment and was not apparent by 62 DAT. CGA-362622 controlled common lambsquarters, common ragweed, Palmer amaranth, sicklepod, smooth pigweed, andIpomoeaspecies including entireleaf, ivyleaf, and pitted morningglory, and the addition of pyrithiobac to the herbicide system, either PRE or POST, increased control ofAmaranthusspecies, jimsonweed, and prickly sida. CGA-362622 did not control jimsonweed or prickly sida. Fluometuron PRE, pyrithiobac PRE, and MSMA plus prometryn LAYBY were beneficial for increasing weed control and cotton lint yields. Prometryn plus MSMA LAYBY increased control of common ragweed, entireleaf morningglory, jimsonweed, pitted morningglory, and smooth pigweed and provided higher cotton yields than similar systems without a LAYBY. The greatest weed control and greatest cotton lint yields required complete weed management systems that included a combination of PRE, POST, and LAYBY treatments.

Microbial Methylation of Metalloids: Arsenic, Antimony, and Bismuth

SUMMARY A significant 19th century public health problem was that the inhabitants of many houses containing wallpaper decorated with green arsenical pigments experienced illness and death. The problem was caused by certain fungi that grew in the presence of inorganic arsenic to form a toxic, garlic-odored gas. The garlic odor was actually put to use in a very delicate microbiological test for arsenic. In 1933, the gas was shown to be trimethylarsine. It was not until 1971 that arsenic methylation by bacteria was demonstrated. Further research in biomethylation has been facilitated by the development of delicate techniques for the determination of arsenic species. As described in this review, many microorganisms (bacteria, fungi, and yeasts) and animals are now known to biomethylate arsenic, forming both volatile (e.g., methylarsines) and nonvolatile (e.g., methylarsonic acid and dimethylarsinic acid) compounds. The enzymatic mechanisms for this biomethylation are discussed. The microbial conversion of sodium arsenate to trimethylarsine proceeds by alternate reduction and methylation steps, with S-adenosylmethionine as the usual methyl donor. Thiols have important roles in the reductions. In anaerobic bacteria, methylcobalamin may be the donor. The other metalloid elements of the periodic table group 15, antimony and bismuth, also undergo biomethylation to some extent. Trimethylstibine formation by microorganisms is now well established, but this process apparently does not occur in animals. Formation of trimethylbismuth by microorganisms has been reported in a few cases. Microbial methylation plays important roles in the biogeochemical cycling of these metalloid elements and possibly in their detoxification. The wheel has come full circle, and public health considerations are again important.

Fruiting Response of Cotton (Gossypium hirsutum) to Pyrithiobac

Field experiments were conducted in 1991 and 1992 near Stoneville, MS and Greenville, MS, to determine the impact of pyrithiobac on cotton fruiting, maturity, and yield. Trials were conducted in areas maintained weed-free with standard production practices to optimize yields. Pyrithiobac was applied at 105 or 210 g ae/ha either PRE or POST to cotton in the cotyledon to 2-leaf, 5- to 7-leaf, and matchhead-square (MHS) stages of growth. At one location, monosodium salt of methylarsonic acid (MSMA) and fluometuron plus MSMA were applied as standard comparisons. At the Stoneville location, injury 1 wk after treatment (WAT) with pyrithiobac ranged from 2.5% with 105 g/ha applied at cotyledon to 2-leaf to 26% with 210 g/ha applied at MHS. Injury was transient in nature and was rarely detectable 4 wk after treatment in either year. Injury was not evaluated at the Greenville location. At Stoneville, a reduction in height occurred with MHS applications of pyrithiobac and MSMA. There was no reduction in yield for any treatment compared to the untreated check in 1991 at Stoneville and in both years at Greenville. In 1992 at Stoneville, treatments of 210 g/ha pyrithiobac, MSMA, and fluometuron plus MSMA at all application timings reduced yield. Pyrithiobac at 105 g/ha applied PRE also reduced yield. Greatest yield loss occurred with treatments of MSMA applied at MHS. There were no yield reductions at either location with postemergence application of 105 g/ha pyrithiobac.

Buffalograss Seedling Tolerance to Postemergence Herbicides

In 1992 and 1993, 12 postemergence herbicide treatments were applied to field-grown buffalograss [Buchloe dactyloides (Nutt.) Engelm.] seedlings having 1 to 3 leaves and 2 to 4 tillers, respectively. The only herbicide treatments that did not cause plant injury at 1 or 2 weeks after treatment (WAT) or reduce turf coverage 4 or 6 WAT compared to nontreated plots (in 1992 or 1993) were (in kg·ha–1) 0.6 dithiopyr, 0.8 quinclorac, 2.2 MSMA, and 0.8 clorpyralid. Evaluated only in 1993, metsulfuron methyl (0.04 kg·ha–1) also caused no plant injury or reduction in coverage. Fenoxaprop-ethyl (0.2 kg·ha–1) caused severe plant injury and reduced coverage by >95% at 6 WAT. Dicamba reduced coverage by 11% at 6 WAT in 1992 but not 1993. The chemicals (in kg·ha–1) triclopyr (0.6), 2,4-D (0.8), triclopyr (1.1) + 2,4-D (2.8), 2,4-D (3.1) + triclopyr (0.3) + clorpyralid (0.2), and 2,4-D (2.0) + mecoprop (1.1) + dicamba (0.2) caused plant injury at 1 or 2 WAT in 1992 or 1993, but coverage was similar to that of nontreated turf by 6 WAT. Chemical names used: 3,6-dichloro-2-pyridinecarboxylic acid (clorpyralid); 3,6-dichloro-o-anisic acid (dicamba); (+/–)-2-[4-(2,4-dichlorophenoxy)phenoxy]propanoic acid (diclofop); 3,5-pyridinedicarbothioic acid, 2-(difluoromethyl)-4-(2-methylpropyl)-6-(trifluoromethyl)-S,S-dimethyl ester (dithiopyr); 2-[4-[(6-chloro-2-benzoxazolyl)oxy]phenoxy] propanoate (fenoxaprop-ethyl); 2-(2,4-dichlorophenoxy)propionic acid (mecoprop); methyl 2-[[[[(4-methoxy-6-methyl-1,3,5-triazin-2-yl)-amino]carbonyl]amino]sulfonyl]benzoate (metsulfuron methyl); monosodium salt of methylarsonic acid (MSMA); 3,7-dichloro-8-quinolinecarboxylic acid (quinclorac); [(3,5,6-trichloro-2-pyridinyl)oxy] acetic acid (triclopyr); (2,4-dichlorophenoxy) acetic acid (2,4-D).