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Fate of cyanobacterial hepatotoxins in artificial recharge of groundwater and in bank filtration
Published in Jos H. Peters, Artificial Recharge of Groundwater, 2020
K. Lahti, J. Vaitomaa, A-L. Kivimaki, K. Sivonen
Both in laboratory and field studies the microcystin concentrations in water were determined by immunoassay (EnvirogardR Microcystins Plate Kit). After repeated freezing at -20 °C and thawing, the samples were filtered through 0.8/0.2 urn membrane syringe filters (Acrodisc, Gelman). Samples of the observation tubes and intake wells were concentrated either by evaporation or in some cases also by filtration through Bond Elut C18 cartridges (Varian USA) according to Harada et al. (1988). The detection limit for total microcystin was 0.01 µg l-1. Samples (1 to 2 litres) were also fractionated and prepared according to Tsuji et al. (1994) for the HPLC analysis. The HPLC equipment and procedures were described by Lahti et al. (1996).
Carbon Nanotubes for A Greener Environment
Published in Ann Rose Abraham, Soney C. George, A. K. Haghi, Carbon Nanotubes, 2023
Divya Radha, N. Rakesh, M. V. Santhosh, K. S. Devaky, Sam John
Besides serving as an excellent adsorbent for the heavy metal ions and dyes, CNTs acts as nanofillers in the reduction of particle concentration in contaminated water. Functionalization of these CNT fillers can make miracles in these applications. Computational studies viz. molecular simulation studies reported that the CNTs could effectively transport water molecules even though they are hydrophobic. The easy frictionless flow of water could be explained by the weaker interactions with water or due to the nanoscale confinement of the tubes that ultimately leads to the narrowing of the energy distribution thereby weakening its interaction with water.35 CNT nanofilters are effectively used in removing the microorganisms like viruses, bacteria, and protozoa. CNTs excellently act as sorbent by retaining these organisms on their surface.36 SWCNTs filters are reported to use for the filtration of Escherichia coli from the water at low pressure.37 SWCNTs immobilized on the ceramic filter were used to enhance the performance of filtration of E. coli. The immobilized CNTs were found to be more robust, thermal resistant, and reusable. Another CNT-based filter prepared by the spray pyrolysis method having a controllable porosity could effectively able to remove the MS2 virus at a low pressure of 8–11 bar.38 CNTs were widely used to remove pollutant microcystins. Microcystins are the toxins produced by the freshwater blue-green algae. The adsorption capacity of CNTs toward these toxins is due to the fitting of molecular dimensions of toxins with the pore size of the CNTs.39
Biological Terrorist Agents
Published in Robert A. Burke, Counter-Terrorism for Emergency Responders, 2017
Saxitoxin acts very quickly and can kill an individual within a few minutes of inhalation of a lethal dose. It acts by blocking nerve conduction directly and causes death by paralyzing muscles of respiration. At slightly less than the lethal dose, the victim may not experience any effects at all. Botulinum toxin needs to invade nerve terminals in order to block the release of neurotransmitters, which under normal conditions control muscle contraction. The symptoms from botulinum toxin are slow to develop (from hours to days) but are just as lethal, causing respiratory failure. This toxin blocks biochemical action in the nerves that activate the muscles necessary for respiration, which leads to suffocation. Unlike saxitoxin, toxicity for botulinum is greater through ingestion than inhalation. Neurotoxins are effective in stopping nerve and muscle function without producing microscopic injury to the tissues, where other toxins directly destroy or damage tissue. Microcystin is a toxin produced by blue-green algae. When it enters the body, it binds to an important enzyme inside the liver cells. No other cells in the body are affected by this toxin. If microcystin is not blocked from reaching the liver within 15–60 minutes of receiving a lethal dose, irreversible damage to the liver will occur. Damage to the liver from this toxin is the same, regardless of the route of exposure. With other toxins, the damage that occurs after contact may vary greatly depending on the route of exposure, even within the same toxin family. Death occurs from ricin because it blocks protein synthesis in many different cells within the body. However, no damage occurs to the lungs unless the route of exposure is inhalation.
Kinetics of catalytic oxidation of the potent aquatic toxin microcystin-LR by latest generation TAML activators
Published in Journal of Coordination Chemistry, 2020
Hannah C. Frame, Yogesh Somasundar, Genoa R. Warner, Alexander D. Ryabov, Terrence J. Collins
Microcystins are toxic cyclic heptapeptides produced by cyanobacteria [11]. Chronic, low-level exposure to microcystins through drinking water is associated with increased rates of cancer in humans [12]. Microcystins damage the liver, neurological and reproductive systems, and are genotoxic [13]. Microcystin-LR (m-LR) containing leucine and arginine residues is among the most toxic [14] and has been detected in natural waters across the United States [15]. Chlorination is a commonly used treatment for microcystin drinking water decontamination but it requires higher than usual concentrations of chlorine to achieve safe levels [16–18], and this brings with it complications of increased toxic chlorinated disinfection by-products [19–21]. An easy-to-use technology, such as TAML/H2O2 catalysis, that is effective in treating m-LR contamination would be of practical interest given the prevalence of this dangerous toxin. In this communication, we report kinetic data related to the unprecedently clean 2/H2O2 oxidation of m-LR under ambient conditions into a single product which then undergoes further slower oxidation.
Response of microcystin biosynthesis and its biosynthesis gene cluster transcription in Microcystis aeruginosa on electrochemical oxidation
Published in Environmental Technology, 2019
Yu Gao, Kazuya Shimizu, Chie Amano, Xin Wang, Thanh Luu Pham, Norio Sugiura, Motoo Utsumi
Microcystin (MC), which is a blue–green algae metabolite, possess tumour-promoting activities and can cause livestock and human death. To date, over 90 analogues of MCs are produced by several genera of cyanobacteria. These analogues represent a family of cyclic heptapeptides with the common structure cyclo (D-Ala-L-X-D-MeAsp-L-Z-Adda-D-Glu-Mdha), where L-X and L-Z are variable amino acids, Adda is 3-amino-9-methoxy-2,6,8,-trimethyl-10-phenyl-4,6-decadienoic acid, D-MeAsp is 3-methyl-aspartic acid and Mdha is N-methyl-dehydroalanine [1]. The presence of the unique Adda amino acid and the cyclic structure renders the resistance to heat, hydrolysis and oxidation of the MCs [2]. The usual major MCs produced by cyanobacteria are MC-RR, MC-YR and MC-LR [3], but experiments on 50% lethal dose in mice have indicated that MC-LR is approximately four times more toxic than MC-RR [4]. Therefore, WHO has set a limit of 1.0 µg L−1 for MC-LR in drinking water.
Involvement of MAPK/ERK1/2 pathway in microcystin-induced microfilament reorganization in HL7702 hepatocytes
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Fei Yang, Cong Wen, Shuilin Zheng, Shu Yang, Jihua Chen, Xiangling Feng
The presence of microcystins (MC) constitutes a threat to the safety of drinking water and public health with consequent adverse effects on humans after entering the body through various ways, including drinking contaminated water, dermal contact, inhalation, consumption of contaminated food, ingestion of algal dietary supplements and hemodialysis (Zurawell et al. 2005). Among all MC, MC-LR has attracted significant attention because this species is the most abundant, extremely toxic, widely distributed, and difficult to remove (Dietrich and Hoeger, 2005; Yang et al. 2014). Recently Zheng et al. (2017) showed that the presence of MC-LR in serum is an independent risk factor for human hepatocellular carcinoma. The International Agency for Research on Cancer (IARC, 2010) classified this toxin as a Group 2B carcinogen.