This paper reviews the main microbial processes involved when toxic metals are removed from wastewater in constructed wetlands. Microbial activity is thought to play a key role in the detoxification of these metals. The paper concentrates on the microbial processes which affect the mobility, the toxicity and bioavailability of metals, namely biosorption, metal sulfide precipitation by sulfate reducers, redox transformations, and methylation, as well as microbe‐plant interactions. These reactions result in either the precipitation and accumulation of metals in wetland soils, or their volatilization and emission into the atmosphere. The possibilities of optimizing the microbially mediated reactions for the development of wetland technology are discussed as a long‐term metal retention strategy.
The basic tendency in the field of plant protection concerns with reducing the use of pesticides and their replacement by environmentally acceptable biological preparations. The most promising approach to plant protection is application of microbial metabolites. In the last years, bactericidal, fungicidal, and nematodocidal activities were revealed for citric, succinic, α-ketoglutaric, palmitoleic, and other organic acids. It was shown that application of carboxylic acids resulted in acceleration of plant development and the yield increase. Of special interest is the use of arachidonic acid in very low concentrations as an inductor (elicitor) of protective functions in plants. The bottleneck in practical applications of these simple, nontoxic, and moderately priced preparations is the absence of industrial production of the mentioned organic acids of required quality since even small contaminations of synthetic preparations decrease their quality and make them dangerous for ecology and toxic for plants, animals, and human. This review gives a general conception on the use of organic acids for plant protection against the most dangerous pathogens and pests, as well as focuses on microbiological processes for production of these microbial metabolites of high quality from available, inexpensive, and renewable substrates.
Microbiological production of physiologically active AA usually used carbohydrates as substrates.Recently, glycerol attracted attention as a promising renewable substrate for biotechnological industry. The effect of pure glycerol on the growth, lipid synthesis, and AA production by earlier selected Mortierella alpina strains LPM-301 and NRRL-A-10995 was studied. It was shown that AA amount varied from 22-29 to 63-68% of lipid in dependence on the initial glycerol concentration in the medium. The transition from glycerol-to nitrogen limitation of the growth was accompanied by a reverse correlation between lipid content of biomass and AA level of lipid. Under selected optimal conditions (nitrogen limitation of fungal growth at glycerol concentrations of 75-81 g/L), AA production by 14-day cultures reached 40-43% of lipid and 11-13% of biomass indicating that glycerol can be successfully used as a carbon substrate for AA production.Practical applications: AA has found wide application in medicine, pharmacology, diet, and infant nutrition as a precursor of several key eicosanoid hormones and pharmacologically active metabolites. It can also be used in agriculture as an elicitor of plant resistance to phytopathogens. Microbiological processes for AA production usually used carbohydrate substrates. Results of this study indicate that AA can be produced from glycerol, which is known as a promising renewable carbon substrate. Under selected optimal conditions (nitrogen limitation of fungal growth at glycerol concentrations of 75-81 g/L), AA production by Mortierella alpina strains LPM-301 and NRRL-A-10995 reached 40-43% of lipid and 11-13% of biomass. These values are comparable with those obtained for carbohydrategrown Mortierella fungi.
The objects of the investigation were: distribution of intracellular magnet-sensitive structures among different taxonomic groups of prokaryotes, localisation and organisation of the magnet-sensitive inclusions (MsI) in cells. The MsI were discovered in representatives of both prokaryotic domains (Bacteria and Archaea), 2 kingdoms and 7 orders of bacteria. They were some amorphous or non-crystalline globules with the electron-transparent centre surrounded with an electron-dense homogenous matrix. The magnetic nature of the structures was shown by attraction with an applied magnet both for the cell suspensions and for the MsI isolated and separated from the destroyed cells. The MsI were studied with transparent electron microscopy and with X-ray analyses. When the cells were grown in the iron-containing nutrient medium, the matrix was enriched with iron. It was shown also that some bacteria grown with cobalt or with chromium contained the cobalt- or chromium-enriched magnetic inclusions.
The placenta is a vitally important organ in the regulation of embryonic development. That is why extensive calcium deposition [also named as pathological placental calcifi cation (PPC)] could have serious negative consequences for the adequate growth of embryos. The nature and mechanism of PPC development has not been defi ned as yet. In the present investigation, we have tested the hypothesis that the molecular basis of PPC development consists of nanobacteria-induced calcifi cation in infected female placenta. Electron microscopy fi ndings support this hypothesis. The initial stage of micro-calcifi cation may originate from the external surface of individual nanobacteria-like particles found mainly in placental extracellular matrix, where initial calcium deposition occurs as a needle surface deposition or as an amorphous-like surface precipitate. Further calcifi c propagation in placenta takes place in the newly formed macro-cavities, which are characterized by low electron density, possibly refl ecting its liquid content around calcium deposition. The micro-cavities contain free nanobacterial-like particles, which may relate to atypical Gram-negative bacteria but not to apoptotic bodies by morphological characters and DNA/RNA distribution. We hypothesize that the increased placental calcifi cation might be caused, at least in part, by nanobacterial infection. [Agababov R M, Abashina T N, Suzina N E, Vainshtein M B and Schwartsburd P M 2007 Link between the early calcium deposition in placenta and its nanobaсterial-like infection;
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