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Toxic cyanobacteria *
Published in Jamie Bartram, Rachel Baum, Peter A. Coclanis, David M. Gute, David Kay, Stéphanie McFadyen, Katherine Pond, William Robertson, Michael J. Rouse, Routledge Handbook of Water and Health, 2015
Anatoxin-a is a low molecular weight secondary amine produced by several species of cyanobacteria (Table 9.1). It mimics acetylcholine – the principal neurotransmitter within the peripheral nervous system and neuro-modulator within the central nervous system. Anatoxin-a has a greater (≈20 times) affinity than acetylcholine for receptors on the post-synaptic membranes of muscles. Unlike acetylcholine however, binding is irreversible and anatoxin-a is not hydrolyzed by acetylcholinesterase (James et al., 2007). Affected muscles continue to be stimulated causing muscular twitching, fatigue and, eventually, paralysis. Intoxication may induce muscle cramping, decreased movement, collapse, exaggerated abdominal breathing, cyanosis, convulsions and paralysis. Severe overstimulation of respiratory muscles can result in rapid death from respiratory arrest and asphyxia. Compared to hepatotoxic cyanotoxins, anatoxin-a is relatively unstable in the environment as it is rapidly degraded by sunlight (oxygen independent photodegradation) and bacteria belonging to genus Pseudomonas. The rapid degradation of anatoxin-a following the collapse of cyanobacterial blooms makes monitoring environmental levels of this toxin difficult. Due to the sporadic occurrence and difficulty monitoring this toxin, few countries have implemented water quality guidelines for anatoxin-a.
Synthesis, Enzyme Localization, and Regulation of Neurosteroids
Published in Sheryl S. Smith, Neurosteroid Effects in the Central Nervous System, 2003
Evers, A.S., Enantioselectivity of pregnanolone-induced gamma-aminobutyric acid(A) receptor modulation and anesthesia, J. Pharmacol. Exp. Ther., 293, 1009-1016, 2000. Zhang, X. and Nordberg, A., The competition of (-)-[3H]nicotine binding by the enantiomers of nicotine, nornicotine and anatoxin-a in membranes and solubilized preparations of different brain regions of rat, Naunyn Schmiedebergs Arch. Pharmacol., 348, 28-34, 1993.Badio, B. and Daly, J.W., Epibatidine, a potent analgetic and nicotinic agonist, Mol. Pharmacol., 45, 563-569, 1994.Abreo, M.A., Lin, N.H., Garvey, D.S., Gunn, D.E., Hettinger, A.M., Wasicak, J.T., Pavlik, P.A., Martin, Y.C., Donnellγ-Roberts, D.L., Anderson, D.J., Sullivan, J.P., Williams, M., Arneric, S.P., and Holladay, M.W., Novel 3-pyridyl ethers with subna-nomolar affinity for central neuronal nicotinic acetylcholine receptors, J. Med. Chem., 39, 817-825, 1996.Demirgoren, S., Majewska, M.D., Spivak, C.E., and London, E.D., Receptor binding and electrophysiological effects of dehydroepiandrosterone sulfate, an antagonist of the GABAA receptor, Neuroscience, 45, 127-135, 1991.Majewska, M.D., Demirgoren, S., Spivak, C.E., and London, E.D., The neurosteroid dehydroepiandrosterone sulfate is an allosteric antagonist of the GABAA receptor, Brain Res., 526, 143-146, 1990.Nilsson, K.R., Zorumski, C.F., and Covey, D.F., Neurosteroid analogues. 6. The synthesis and GABAA receptor pharmacology of enantiomers of dehydroepiandrosterone sulfate, pregnenolone sulfate, and (3-alpha,5-beta)-3-hydroxypregnan-20-one sulfate, J. Med. Chem., 41, 2604-2613, 1998.Weaver, C.E., Jr., Marek, P., Park-Chung, M., Tam, S.W., and Farb, D.H., Neuropro-
Cyanotoxin genotoxicity: a review
Published in Toxin Reviews, 2022
Serkan Yilmaz, Taha Gökmen Ülger, Bayram Göktaş, Şahlan Öztürk, Duygu Öztaş Karataş, Ebru Beyzi
The most studied group of cyanotoxins is microcystins (MC) which known as liver toxins; anatoxin-a and saxitoxins show strong neurotoxic effects (McLellan and Manderville 2017). Cylindrospermopsin (CYN), which is one of the hazardous cyanotoxin in fresh water sources worldwide, is highly resistant to light, temperature and pH conditions and has cytotoxic, hepatotoxic and genotoxic effects (De La Cruz et al. 2013). CYN can be produced by a large number of cyanobacteria, which can be released into the environment at significantly higher extracellular concentrations compared to MC (Boopathi and Ki 2014). Therefore, it is one of the most widely distributed cyanotoxins detected in water bodies in tropical, subtropical and even temperate regions. In US EPA Contaminant Candidate List 3, the safety value of CYN for drinking water has been determined as 1 µg L−1 (Munoz et al. 2019). The tolerable daily intake level for MC and CYN is stated as 0.04 and 0.03 μg kg−1 body weight (Diez-Quijada Jiménez et al. 2020).
An overview on cyanobacterial blooms and toxins production: their occurrence and influencing factors
Published in Toxin Reviews, 2022
Isaac Yaw Massey, Muwaffak Al osman, Fei Yang
Anatoxin-a is a small alkaloid and potent neurotoxin promoter. It is a bicylic secondary amine, smallest cyanotoxin, and has a molecular weight of 165 Da. Osswald et al. (2007) indicated that Anabaena sp., Aphanizomenon sp., Microcystis sp., Oscillatoria sp., Arthrospira sp., Raphidiopsis sp., Planktothrix sp., Phormidium sp., Nostoc sp. and Cylindrospermum sp. are capable to produce this toxin. The amine pKa value of 9.4 renders the cationic form of anatoxin-a the most prevalent form in natural waters and its oxidation may be pH-dependent. Homoanatoxin-a with an additional methylene unit on its side chain has been identified as a variant of anatoxin-a (Skulberg et al.1992). Anatoxin-a is a potent nicotinic agonist capable of producing neuromuscular blockade leading to paralysis and eventually death owing to respiratory arrest (Fawell et al.1999, Osswald et al.2007). Although anatoxin-a is not considered widespread as the cyclic peptide hepatotoxins, it is documented to have caused animal poisonings in some parts of the world identified (Fawell et al.1993, Sivonen and Jones 1999, Svircev et al.2019). Due to the toxic consequences, Fawell et al. (1999) recommended 1 µg/L anatoxin-a concentration to provide significant water safety since no official drinking water guideline is established.
Use of proteomics to detect sex-related differences in effects of toxicants: implications for using proteomics in toxicology
Published in Critical Reviews in Toxicology, 2018
Ivonne M. C. M. Rietjens, Jacques Vervoort, Anna Maslowska-Górnicz, Nico Van den Brink, Karsten Beekmann
For other compounds studied there was no upfront evidence for sex-specific responses to toxicant exposure (reflected by a “-” in column 5 Table 1). These studies were initiated to find new biomarkers or elucidate a possible mode of action. In some cases the possible mode of action would unlikely be sensitive to sex-differences. This is the case for example for neurotoxins like anatoxin-a (Carneiro et al. 2015) and 4,5-dichloro-2-n-octyl-4-isothiazolin-3-one (DCOIT) (Chen et al. 2014), the metalloid arsenic (Carlson et al. 2013), or benzo[a]pyrene (B[a]P) (Riva et al. 2011). Anatoxin-a exerts its toxic effects by acting as a competitive agonist for acetylcholine receptors affecting signal transmission in neuromuscular junctions. DCOIT decreases acetylcholinesterase activity resulting in potential neurotoxicity. Such modes of action have no upfront reason to result in sex-dependent differences. One could rather argue that for such modes of action effects on protein abundance patterns will be secondary to the toxicity and not really involved in the mode of action underlying the adverse effects. The mode of action of the metalloid arsenic is less well defined but evidence for sex-specific adverse effects has not been reported, resulting in a decision of other researchers to even combine the sexes in the same group in a study on serum proteomic profiling of chronic arsenic exposure in humans (Zhao et al. 2010). Also for pentachlorophenol (PCP) which is a potent uncoupler of oxidative phosphorylation, differential responses in males and females as observed by Fang et al. (2010) would not easily be explained by a sex-specific mode of action, although it can be foreseen that the hydroxyl moieties in PCP and/or its metabolites may facilitate binding to hormone receptors (Danzo 1997).