scholarly journals ANATOXIN-A(S): NATURAL ORGANOPHOSPHORUS ANTICHOLINESTERASE AGENT

2011 ◽  
Vol 80 (3) ◽  
pp. 129-139 ◽  
Author(s):  
Jiří Patočka ◽  
Ramesh C. Gupta ◽  
Kamil Kuča
1998 ◽  
Vol 3 (1) ◽  
Author(s):  
NEUZA MARIA FERRAZ DE MELLO GONÇALVES ◽  
WILMA P. BASTOS-RAMOS ◽  
METRY BACILA

Foi levada a efeito um estudo sobre a sensibilidade do peixe antártico Notothenia neglecta ao agente anticolinesterásico não poluente Malathion [O-O-dimetil S-(1,2-dicarbetoxietil) fosforoditioato]. Especimens de N. neglecta foram injetados com Malathion em doses de 15 ou 30 mg/kg de peso corpóreo e observados durante dez dias. O experimento foi monitorado pela determinação da atividade anticolinesterásica sérica bem como pela observação da depressão respiratória, pelo comportamento catatônico dos animais, pela mudança da coloração corpórea e pelas respostas colinérgicas muscarínicas. Os resultados desse experimento mostraram que a N. neglecta é significantemente mais sensível ao Malathion do que o peixe de água doce Oreochomis niloticus. Ao final do experimento todo o material utilizado foi cuidadosamente embalado e transportado para nossos laboratórios no Brasil. Abstract A research has been carried out on the sensitivity of the Antarctic fish Notothenia neglecta towards the non-pollutant anticholinesterase agent Malathion [O,O-dimethyl S-(1,2-dicarbethoxyethyl) phosphorodithioate]. Specimens of N. neglecta were injected with Malathion in doses of 15 or 30 mg/kgbw and observed regarding their behavior, somatic and physiological responses during ten days. They were monitored by the assay of serum cholinesterase activity as well as by the observation of respiratory depression and by the catatonic behavior, changes of body color and cholinergic muscarinic responses. Results of this experiment showed that N. neglecta is significantly more sensitive to Malathion as compared to the fresh water fish Oreochomis niloticus. At the end of the experiment all waste material was packed up and carried to our laboratories back home.


1950 ◽  
Vol 33 (6) ◽  
pp. 904-908 ◽  
Author(s):  
W.G. Marr ◽  
David Grob

1978 ◽  
Vol 57 (5-6) ◽  
pp. 748-751 ◽  
Author(s):  
Bogoslav V. Vasic ◽  
Milenko P. Milosevic ◽  
Milorad R. Terzic

The effects of obidoxime, a pyridinium oxime, on the cholinesterase activity and acetylcholine content of the submandibular glands of rats poisoned with armin, an organophosphorus anticholinesterase agent, were studied. The results indicate that obidoxime-induced reactivation of phosphorylated cholinesterase can suppress completely the increase in the concentration of acetylcholine that develops within the submandibular gland after administration of armin alone.


1975 ◽  
Vol 43 (6) ◽  
pp. 689-705 ◽  
Author(s):  
Minoru Aoyagi ◽  
John Stirling Meyer ◽  
Vinod D. Deshmukh ◽  
Erwin O. Ott ◽  
Yukio Tagashira ◽  
...  

✓ Cerebral autoregulation and vasomotor responsiveness to carbon dioxide (CO2) were measured quantitatively by the use of the autoregulation index and chemical index, respectively, in normal baboons before and after intravertebral and intracarotid infusion of the anticholinesterase agent, neostigmine methylsulfate (Prostigmin). Continuous measurements were made of cerebral blood flow (measured as bilateral internal jugular venous outflow), arterial and cerebral venous pO2 and pCO2, cerebral arteriovenous oxygen differences, and endotracheal CO2. The effect of intravertebral infusion of neostigmine (12.5 µg/kg body weight) was compared to intracarotid infusion of neostigmine (25 µg/kg body weight) for assessment of any specific action of the drug on a hypothetical cholinergic vasomotor center, presumed to be located in the territory of the vertebrobasilar supply. No significant or persistent changes in cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) followed either intravertebral or intracarotid infusion of neostigmine. Cerebral vascular resistance (CVR) and cerebral perfusion pressure (CPP), however, decreased significantly after intravertebral infusion. Cerebral autoregulatory vasoconstriction during increases of CPP was significantly reduced following both intravertebral and intracarotid infusion. Cerebral autoregulatory vasodilatation was not altered as CPP was lowered. Cerebral vasodilatory reactivity to CO2 inhalation was significantly enhanced following intravertebral neostigmine but not following intracarotid neostigmine. Cerebral vasoconstrictive response to hyperventilation was not influenced by neostigmine. These results support the view that central cholinergic cerebrovascular influences exist, and are vasodilatory in nature.


1995 ◽  
Vol 14 (1) ◽  
pp. 49-54 ◽  
Author(s):  
Michel Hubert ◽  
Dominique Lison

1. Pyridostigmine (PYR) pretreatment is used by the mili tary to obtain 20—30% whole blood acetylcholinesterase (AChE) inhibition in order to enhance the effectiveness of the standard therapeutic regimen for poisoning by an organophosphate anticholinesterase agent. The present study was undertaken to investigate in a rat model the potential muscle damage produced by this pretreatment when given alone or combined with physical exercise. 2. Grip strength and biochemical measurements, i.e. serum creatine phosphokinase (CPK) activity and creatine urinary excretion rate, together with histological studies, were performed in resting animals during a period of 14 days of PYR administration in a dose producing 20-30% whole blood acetylcholinesterase inhibition. No evidence was found of a deleterious effect of this treatment on the skeletal muscle. 3. In contrast, following physical exercise, the same treat ment significantly exacerbated the biochemical changes reflecting a loss of integrity in skeletal muscles, namely, increased CPK and urinary creatine excretion rate. The significance of this observation remains to be clarified.


1993 ◽  
Vol 21 (2) ◽  
pp. 261-268
Author(s):  
Thomas W. Sawyer ◽  
M. Tracy Weiss ◽  
Angela Bianco

The anticholinesterase activity of the carbamate insecticides, carbofuran and aldicarb, was examined in primary cultures of chick embryo forebrain neurons. Both compounds inhibited acetylcholinesterase, with carbofuran being more potent than aldicarb by more than two orders of magnitude. Preincubation of carbofuran with hepatic S9, derived from rat or chick, decreased its anticholinesterase activity, with chick S9 exerting the greater deactivating effect. Conversely, preincubation of aldicarb with rat control S9 increased its anticholinesterase activity, while chick S9 had only a slight effect. Preincubation of the test compounds with S9 obtained from animals induced with phenobarbitone or 3-methylcholanthrene generally had a slightly deactivating effect, with the exception of aldicarb, where preincubation with induced rat hepatic S9 fractions slightly increased its potency as an anticholinesterase agent when compared to the effects of control S9. Preincubation of aldicarb and carbofuran with hepatic S9 fractions from both rat and chick altered their anticholinesterase activities, so that they were more predictive of their relative potential species toxicities in vivo. The relative toxicities of aldicarb and carbofuran, within a given species, however, were not as well predicted. This model may be of use in assessing the potential toxicities of carbamate pesticides with respect to species differences.


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