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Evaluation of Water and Its Contaminants
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
Toxic effects from anatoxin-a progress very rapidly because it acts directly on the nerve cells (neurons) as a neurotoxin. The progressive symptoms of anatoxin-a exposure are loss of coordination, twitching, convulsions, and rapid death by respiratory paralysis. The nerve tissues which communicate with muscles contain a receptor called the nicotinic acetylcholine receptor. Stimulation of these receptors causes a muscular contraction. The anatoxin-a molecule is shaped so it fits this receptor, and in this way it mimics the natural neurotransmitter normally used by the receptor, acetylcholine. Once it has triggered a contraction, anatoxin-a does not allow the neurons to return to their resting state, because it is not degraded by cholinesterase which normally performs this function. As a result, the muscle cells contract permanently, the communication between the brain and the muscles is disrupted, and breathing stops (Figure 3.40).657,658
Laboratory analysis of cyanobacterial toxins and bioassays
Published in Ingrid Chorus, Martin Welker, Toxic Cyanobacteria in Water, 2021
Linda A. Lawton, James S. Metcalf, Bojana Žegura, Ralf Junek, Martin Welker, Andrea Törökné, Luděk Bláha
The most commonly used analytical system for the detection, identification and quantification of anatoxin-a is HPLC-PDA or LC/MS(MS). The advantage of ultra-performance liquid chromatography (UPLC) columns and systems is that they allow short retention times, providing a rapid analysis. One of the main challenges for the analysis of anatoxin-a is the ubiquitous co-occurrence of phenylalanine, which has a very similar retention time and mass. It is important to ensure that the selected chromatography column and elution profile can separate the two compounds (see Box 5.3 for an example of this misinterpretation of analytical results).
An ecotoxicological assessment of the acute toxicity of anatoxin congeners on New Zealand Deleatidium species (mayflies)
Published in Inland Waters, 2020
Laura T. Kelly, Jonathan Puddick, Ken G. Ryan, Olivier Champeau, Susanna A. Wood
Anatoxins inhibit photosynthesis and reduce pigment production in some macrophytes (e.g., Lemna minor and Cladophora fracta; Mitrovic et al. 2004, Kaminski et al. 2016), although these effects occur at anatoxin concentrations higher than those typically measured in environmental samples. In some chlorophytes (e.g., Selenastrum capricornutum), anatoxin exposure in concert with microcystins has been shown to promote growth (Chia et al. 2019). Some freshwater fish (e.g., Oncorhynchus mykiss and Cyprinus carpio) accumulate anatoxins following exposure to anatoxin-contaminated water (Osswald et al. 2007, 2011). Information on the effects of anatoxins on invertebrates is scarce. Osswald et al. (2008) showed that marine mussels can accumulate anatoxins, and Macallan et al. (1988) showed anatoxin-a can bind to receptors from locust tissue. Invertebrates have nicotinic acetylcholine receptors (nAChRs) in their nervous systems (Macallan et al. 1988), and because anatoxins interact with these receptors (Macallan et al. 1988), acute toxicity effects may be evident through inhibition of the major excitatory system. Crude cyanobacterial extracts containing anatoxins have been utilised in invertebrate toxicity assays, resulting in considerable mortality (Anderson et al. 2018). A single study examining the acute toxicity of purified anatoxin-a identified much lower toxicity than crude cyanobacterial extracts in Chironomus spp. larvae (Toporowska et al. 2014). To our knowledge, this study is the first to examine the acute effects of purified anatoxins on benthic macroinvertebrates. This critical gap is a concern because invertebrates comprise an important component of aquatic ecosystems.