Vanadium-induced inhibition of renal Na+, K+-adenosinetriphosphatase in the chicken after chronic dietary exposure.
Recent work has shown that V accumulates in the kidney and is a potent inhibitor of Na+, K+-adenosinetriphosphatase (ATPase) in vitro. Thus, as a nutritionally required element, V may regulate cation transport. The effect of chronic intake of the metal on Na+, K+-ATPase in vivo has not been reported. In this study laying strain chickens were fed calcium orthovanadate for 15 mo from d 1 of age at levels of 0, 25, 50, and 100 ppm in the diet. Whole tissue homogenates and 13,000 X g fractions were analyzed for ATPase activities. Concentrations of V producing 50% inhibition of Na+, K+-ATPase activity ranged from 1.0 X 10(-5) M in liver to 1.8 X 10(-6) M in kidney, which was the most sensitive tissue tested in vitro. Mg2+ -ATPase was more resistant to V than Na+, K+-ATPase. Studies in vivo suggested a V-dependent inhibition of renal Na+, K+-ATPase. Correlation of enzyme specific activity and levels of V in kidneys suggested V-ATPase mediated alteration in renal function.
D000251:Adenosine Triphosphatases / Q000378:metabolism; D000818:Animals; D017301:Ca(2+) Mg(2+)-ATPase; D002645:Chickens; D004032:Diet; D005260:Female; D007668:Kidney / Q000032:analysis / Q000187:drug effects / Q000378:metabolism*; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors* / Q000378:metabolism; D014638:Vanadates; D014639:Vanadium / Q000032:analysis / Q000494:pharmacology*
D014639:Vanadium; D014638:Vanadates; D000251:Adenosine Triphosphatases; D017301:Ca(2+) Mg(2+)-ATPase; D000254:Sodium-Potassium-Exchanging ATPase