Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thiobencarb (S-(4-chlorobenzyl)-N,N-diethyl thiol carbamate), a dithiocarbamate herbicide, was found to cause neuronal dysfunction in adult and neonate albino rats. In general, organocarbamates exert their action by inhibiting acetylcholinesterase (AChE) activity. Thiobencarb inhibited both acetylcholinesterase and adenosine triphosphatase (ATPase) activities in rat brain. Withdrawal of thiobencarb treatment resulted in the recovery of AChE activity to a normal level, whereas there was no recovery of Na(+)-K(+)-ATPase activity in either neonate or adult rat brains. The results suggest that neuronal dysfunction caused by thiobencarb is mainly due to the inhibition of ATPase activity rather than to the inhibition of AChE activity.
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PMID:Comparative study on the changes in AChE and ATPase activities in neonate and adult rat brains under thiobencarb stress. 844 Aug 73

European eels (Anguilla anguilla) were exposed to a sublethal thiobencarb concentration of 0.22 mg/L in a flow-through system for 96 h. Mg(2+) and Na(+)-K(+) adenosine triphosphatase (ATPase) activities were evaluated in gill and muscle tissues at 2, 12, 24, 48, 72, and 96 h of thiobencarb exposure. Gill ATPase activities were rapidly inhibited from 2h of contact onward. Highest inhibition was registered for Na(+), K(+)-ATPase (85%) from 2 to 12h. Both Mg(2+) and total ATPase were inhibited (>73%) during the first hours of toxicant exposure. At the end of the exposure period (96 h) ATPase activities were still different from those of the controls (>50%). Significant inhibition was detected in Na(+), K(+)-ATPase activity (80%) in muscle tissue after 2h and it was maintained over the entire exposure time. However, Mg(2+)-ATPase and total ATPase showed only perturbations after 2 h of exposure. Eels were exposed to 0.22 mg/L of thiobencarb for 96 h and then a recovery period in herbicide-free water was allowed for 192 h. Gill and muscle samples were removed at 8, 24, 72, 96, 144, and 192 h and ATPase activity was evaluated. Following 144 h of recovery, Mg(2+)- and Na(+), K(+)-ATPase activities, as well as total ATPase activity, in gills of those animals previously exposed to 0.22 mg/L of thiobencarb were still significantly different compared to controls. Thiobencarb seems to act to alter the ionic profiles. Since ion-dependent ATPases are known to regulate the influx and efflux of ions across the membrane to maintain the physiological requirements of the cells, the inhibition of Na(+), K(+)-ATPase probably induced osmoregulatory perturbations. On the other hand, thiobencarb exposure causes increases in the muscle water content of A. anguilla. The results indicated that water content increased significantly (>100% higher than the controls) during the first 24 h of exposure.
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PMID:Eel ATPase activity as biomarker of thiobencarb exposure. 1457 84