Toxicology and Pharmacological Action of
            <i>Anabaena flos-aquae</i>
            Toxin

Carmichael, Wayne W.; Biggs, David F.; Gorham, Paul R.

doi:10.1126/science.803708

Cited by 257 publications

(110 citation statements)

References 1 publication

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“…1977). This toxin is produced in freshwater algal blooms and is responsible for the death of livestock and waterfowl via a depolarizing blockade of neuromuscular transmission and subsequent respiratory paralysis (Carmichael et al, 1975). Anatoxin-A is found to be a stereospecific agonist of nicotinic receptors in frog muscle and torpedo electric organs (Swanson et al, 1986).…”

mentioning

confidence: 99%

Cardiovascular effects of anatoxin-A in the conscious rat

Sirén

Feuerstein

1990

Toxicology and Applied Pharmacology

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Cardiovascular Effects of Anatoxin-A in the Conscious Rat. SJREN, A.-L., AND FEUERSTEIN, G. (1990). Toxicol. Appl. Pharmacol. 102,91-100. The effects ofanatoxin-A on mean arterial pressure (MAP), heart rate, cardiac index (CI), and blood flow (BF) in hindquarter (HQ), renal (R). and mesenteric (M) vascular beds were studied after intravenous (iv) and intracerebroventricular (icv) administration in the conscious rat. The pharmacological profile of anatoxin-A was further compared to nicotine administered iv and icv. MAP and heart rate were measured from femoral artery, CI by thermodilution method, and blood flow by Doppler velocimetry. Anatoxin-A and nicotine (30, 100 and 300 1-!g/kg iv) produced an increase in MAP with concomitant bradycardia. The highest doses increased Cl. MBF and RBF decreased due to a vasoconstriction in M and R vasculature. These effects were attenuated by the ganglion blocker chlorisondamine (5 mg/kg, iv). Anatoxin-A ( 100 1-!g/k~ iv) increased plasma epinephrine Ievels by 2-fold with virtually no effect on norepinephrine whereas nicotine ( 100 ~oLg/kg, iv) increased plasma epinephrine and norepinephrine by 20-to 30-fold. Central administration of anatoxin-A and nicotine (30-100 ,ug/kg icv) increased MAP with no effect on heart rate and produced M and R vasoconstriction. In summary, the present study demonstrates that anatoxin-A acts as a nicotinic cholinergic agonist in the c.onscious rat after both systemic and centrat administration. Anatoxin-A and nicotine produced pressor and reno-splanchnic vasoconstrictor responses and at high doses increased cardiac output. These effects were mediated by activation ofthe nicotinic receptors in the adrenal medulla and sympathetic ganglia. However, marked differences were found in the potency ofanatoxin-A versus nicotine to stimulate the sympathoadrenomedullary axis. ti;l 1990 Academic Press,lnc.

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mentioning

confidence: 99%

Cardiovascular effects of anatoxin-A in the conscious rat

Sirén

Feuerstein

1990

Toxicology and Applied Pharmacology

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“…The severe hypoxia observed in the present experiment may be brought about by the direct effect of AnTx-a on the respiratory muscles and the diaphragm, resulting in paralysis. This conclusion is supported by studies of CARMICHAEL et al (1975) and VALENTINE et al (1991). Generally, hypoxia is associated with interactions between reflex, nerve-mediated responses, and local inftuence of blood gas tension changes, e.g.…”

Section: Discussionmentioning

confidence: 72%

Cardio-respiratory changes and mortality in the conscious rat induced by (+)- and (±)-anatoxin-a

Adeyemo

Sirén

1992

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“…(33,36,37). Anatoxin-a exerts its neurotoxic effect by mimicking acetylcholine with an LD50 of 200-250 pg/kg bw (36). Anatoxina(s) is the only naturally occurring organophosphate and has been isolated from A. flos-aquae and A. lemmermannii (38).…”

Section: Cylindrospermopsinmentioning

confidence: 99%

“…and in small amounts even in Microcystis sp. (33,36,37). Anatoxin-a exerts its neurotoxic effect by mimicking acetylcholine with an LD50 of 200-250 pg/kg bw (36).…”

Section: Cylindrospermopsinmentioning

confidence: 99%

Cyanobacterial toxins: removal during drinking water treatment, and human risk assessment.

Hitzfeld

Höger

Dietrich

2000

Environ Health Perspect

257

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Cyanobacteria (blue-green algae) produce toxins that may present a hazard for drinking water safety. These toxins (microcystins, nodularins, saxitoxins, anatoxin-a, anatoxin-a(s), cylindrospermopsin) are structurally diverse and their effects range from liver damage, including liver cancer, to neurotoxicity. The occurrence of cyanobacteria and their toxins in water bodies used for the production of drinking water poses a technical challenge for water utility managers. With respect to their removal in water treatment procedures, of the more than 60 microcystin congeners, microcystin-LR (L, L-leucine; R, L-arginine) is the best studied cyanobacterial toxin, whereas information for the other toxins is largely lacking. In response to the growing concern about nonlethal acute and chronic effects of microcystins, the World Health Organization has recently set a new provisional guideline value for microcystin-LR of 1.0 pg/L drinking water. This will lead to further efforts by water suppliers to develop effective treatment procedures to remove these toxins. Of the water treatment procedures discussed in this review, chlorination, possibly micro-/ultrafiltration, but especially ozonation are the most effective in destroying cyanobacteria and in removing microcystins. However, these treatments may not be sufficient during bloom situations or when a high organic load is present, and toxin levels should therefore be monitored during the water treatment process. In order to perform an adequate human risk assessment of microcystin exposure via drinking water, the issue of water treatment byproducts will have to be addressed in the future.

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Toxicology and Pharmacological Action of Anabaena flos-aquae Toxin

Cited by 257 publications

References 1 publication

Cardiovascular effects of anatoxin-A in the conscious rat

Cardiovascular effects of anatoxin-A in the conscious rat

Cardio-respiratory changes and mortality in the conscious rat induced by (+)- and (±)-anatoxin-a

Cyanobacterial toxins: removal during drinking water treatment, and human risk assessment.

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