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Cyanobacteria toxic effects

Certain strains of cyanobacteria produce toxins. These cyanobacterial toxins can be classified according to their chemical structure or their toxicity. Table 16.1 summarises the characteristics of the main cyanobacterial toxins. Depending on the chemical structure, there are cyclic peptides, alkaloids and lipopolysaccharides. According to the toxic effects, they are classified as ... [Pg.331]

Some blue-green algae or cyanobacteria can also produce a range of algal toxins that can cause harmful health effects from skin irritation, liver damage, tumor promotion, and death by nerve damage if consumed in sufficient quantity. Detailed information on the structures, occurrence, and toxic effects of these compounds can be found in Yoo et al. [62]. [Pg.696]

In contrast to the toxic effects of arsenic, some prokaryotic (anaerobic) bacteria depend upon arsenic. Mono Lake, California, is a closed, saline basin (i.e. no water outlet) that is fed by freshwater streams and underwater springs including volcanic sources. In 2008, researchers discovered that cyanobacteria and photosynthetic, prokaryotic bacteria in Mono Lake use arsenic(III) compotmds as their only photosynthetic electron donor. The process converts As(III) to As(V). The discovery may he relevant to an understanding of the arsenic cycle on ancient Earth in which oxygen played no role. [Pg.487]

The toxins produced by freshwater cyanobacteria can be classified based on their toxic effects, their molecular... [Pg.421]

The ability to identify and quantify cyanobacterial toxins in animal and human clinical material following (suspected) intoxications or illnesses associated with contact with toxic cyanobacteria is an increasing requirement. The recoveries of anatoxin-a from animal stomach material and of microcystins from sheep rumen contents are relatively straightforward. However, the recovery of microcystin from liver and tissue samples cannot be expected to be complete without the application of proteolytic digestion and extraction procedures. This is likely because microcystins bind covalently to a cysteine residue in protein phosphatase. Unless an effective procedure is applied for the extraction of covalently bound microcystins (and nodiilarins), then a negative result in analysis cannot be taken to indicate the absence of toxins in clinical specimens. Furthermore, any positive result may be an underestimate of the true amount of microcystin in the material and would only represent free toxin, not bound to the protein phosphatases. Optimized procedures for the extraction of bound microcystins and nodiilarins from organ and tissue samples are needed. [Pg.120]

Neurotoxins, such as saxitoxin and anatoxin-a, have been implicated in mediating competitive interactions between toxic cyanobacteria and other photoautotrophs, but few studies have explicitly examined the allelopathic effects of these compounds (e g., Kearns and Hunter 2001). Although it is reasonable to assume that these compounds bind to algal and cyanobacterial sodium channels in a similar fashion as in vertebrate neurons, support for this hypothesis is currently lacking. [Pg.113]

DeMott WR, Moxter F (1991) Foraging on cyanobacteria by copepods responses to chemical defenses and resource abundance. Ecology 72 1820-1834 DeMott WR, Zhang Q, Carmichael WW (1991) Effects of toxic cyanobacteria and purified toxins on the survival and feeding of a copepod and three species of Daphnia. Limnol Oceanogr 36 1346-1357... [Pg.116]

In recent years, the unicellular nature of planktonic algae has been exploited for the construction of whole-cell based biosensors capable of real-time response on critical change of the aquatic ecosystems caused by pollutant emissions. Most of the proposed devices are based on the electrochemical detection of the inhibiting effect on the photosynthetic activity of algae and cyanobacteria exerted by some toxicants. [Pg.182]

Claska, M.E., and Gilbert, J. J. 1998. The effect of temperature on the response of Daphnia to toxic cyanobacteria. Freshwat Biol 39, 221-232. [Pg.154]

The herbicidal effect of paraquat is attributable to the formation of superoxide anion (02 ). Superoxide anion is very toxic compound and is formed by the reaction of oxygen with paraquat radical (paraquat ). Plants, algae, and cyanobacteria have ferredoxin-NADP reductase to form NADPH for the reduction of carbon dioxide (see below). The chemolithoautotrophs also have NAD(P) (NAD and NADP) reductase to form NAD(P)H for the reduction of carbon dioxide. Paraquat [mid-point redox potential at pH 7.0 (Emj 0) = -0.43 V] radical is produced when paraquat is reduced by the catalysis of ferredoxin-NAD(P) reductase or NAD(P) reductase, which catalyzes the reduction of many compounds with of around -0.4 V. Although the aerobic organisms (and even many anaerobic organisms) have superoxide dismutase (SOD) which detoxifies superoxide anion in cooperation with catalase [ascorbate peroxidase in the case of plants (Asada, 1999)], the anion accumulates in the organisms when it is over-produced beyond the capacity of SOD. [Pg.43]


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See also in sourсe #XX -- [ Pg.421 ]




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Toxic cyanobacteria

Toxic effects

Toxicity effective

Toxicity/toxic effects

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