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)

Acute renal failure was induced in rats by injection of a lethal dose of live Escherichia coli. Enzyme activities of the proximal tubule were studied histochemically at three, six, and 12 hours following E coli injection. The enzymes examined were alkaline phosphatase (A1Pase), acid phosphatase (AcPase), adenosine triphosphatase (ATPase), succinate dehydrogenase (SDH), glucose-6-phosphatase (G6Pase), and glucose-6-phosphate dehydrogenase (G6PDH). At three hours, ATPase activity was slightly decreased, while other enzymes showed no changes in activities at this time. At six hours, a slight increase in AcPase activity was seen in the pars recta. At this time, although A1Pase showed no change in activity, other enzymes revealed slight decreases in activities: G6Pase and SDH in the pars convoluta, ATPase in the pars convoluta and pars recta, and G6PDH in pars recta. At 12 hours after treatment, all enzymes showed decreases in activities; however, no necrotic tubule changes were detectable by light microscopy. Since sodium reabsorption in proximal tubules requires a sodium pump consisting of Na-K ATPase, early histochemical changes in ATPase activity in proximal tubule following bacteremia may be related to early changes in sodium reabsorption causing polyuria and to the subsequent development of acute renal failure.
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PMID:The pathophysiology of septic shock: acute renal failure in rats following live E coli injection. A histochemical study of the proximal tubules. 629 45

An initial event in gram-negative bacteremia is activation of the complement cascade with production of C5a. C5a, in turn, acts as a chemotactic stimulus for leukocytic aggregation and, in conjunction with bacterial products, stimulates the release of oxygen free radicals from leukocytes. We have hypothesized that these oxygen free radicals (.O2-, superoxide anion; .OH, hydroxyl radical; H2O2, hydrogen peroxide) contribute to the characteristic myocardial dysfunction of endotoxin shock, Isolated canine cardiac sarcoplasmic reticulum (SR) was used as a subcellular determinant of mechanical function. SR was incubated for 20 min at 37 degrees C in the presence of phorbol myristate acetate activated leukocytes (A-L) and calcium uptake and Ca2+-adenosine triphosphatase (ATPase) activities were measured. Activated leukocytes significantly depressed SR Ca2+ uptake rates (C = 1.12 +/- 0.05 mumol CA2+/mg-min; A-L = 0.73 +/- 0.05). The addition of catalase (CAT; 10 micrograms/ml) or superoxide dismutase (SOD: 10 micrograms/ml) plus CAT reversed the inhibition of SR Ca2+ uptake. SOD further depressed SR Ca2+ uptake (+SOD = 0.55 +/0 0.04 mumol Ca2+/mg-min). Mannitol had no effect. SR ATPase activity was inhibited with A-L (C = 1.41 +/- 0.04 mumol Pi/mg-min; A-L = 0.84 +/- 0.09). Neither mannitol, nor SOD nor CAT alone had any effect on the depression of SR ATPase activity. SOD plus CAT reversed the ATPase depression induced by A-L. It is concluded that phorbol myristate acetate activated leukocytes via free radical-mediated mechanisms can directly affect function and activity of the excitation-contraction coupling system of cardiac muscle. Free radical scavengers identified hydrogen peroxide as a major mediator of depressed Ca2+ uptake rates. In conjunction with the superoxide anion, hydrogen peroxide contributes to the depressed ATPase activity.
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PMID:Interaction of oxygen free radicals and cardiac sarcoplasmic reticulum: proposed role in the pathogenesis of endotoxin shock. 685 Oct 3