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)

Cells of sarcoma 180 and of Ehrlich's carcinoma were maintained by serial transplantation in male and female Swiss mice. Either estrogen, progesterone, or testosterone were injected im at doses of 1 mg/mouse. Ascitic fluid was aspirated at intervals of 1, 3, 6, 24, and 48 hours following hormone injections. Enzyme activities were analyzed by subjective grading according to the intensity of staining reaction. Estrogen produced enhancement of alkaline phosphatase activity in both types of cells in both sexes of mice. Progesterone produced increased alkaline phosphatase activity in both types of cells from female hosts but an inhibitory effect in male hosts' cells. Testosterone produced no change in enzyme activity in tumor cells of female hosts but in male hosts it inhibited enzyme activity of sarcoma 180 cells and activated activity in carcinoma cells. The effect of all 3 hormones on acid phosphatase activity was activation. With adenosine triphosphatase, estrogen stimulated the activity in both types of tumor in both sexes. Progesterone stimulated cells from male hosts with little or no effect on cells from female hosts. This enzyme was resistant to testosterone. Succinate dehydrogenase activity under similar conditions was different. Estrogen reduced this activity and progesterone produced some inhibition of activity. Testosterone inhibited the sarcoma cells but had no effect on carcinoma cells of either sex. Others have shown that sex hormones affect the enzyme activities beyond the target tissues, particularly in the liver, kidney, and pancreas. Different responses of the enzymes seemed to depend on the endogenous hormonal status of the mice.
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PMID:Enzymatic responses of transplanted tumour cells towards estrogen, progesterone and testosterone. 13 8

The effect of estrogen on plasma membrane was investigated using the primary cultured rat hepatocytes treated with carbon tetrachloride (CCl4) and the isolated plasma membrane of rat liver. 17 beta-Estradiol (E2), at concentrations of 10(-10) M to 10(-4) M, 10(-8) M to 10(-6) M and 10(-12) M to 10(-4) M, had an inhibitory effect on the CCl4-induced leakage of glutamic oxaloacetic transaminase, glutamic pyruvic transaminase and lactate dehydrogenase, respectively from primary cultured rat hepatocytes. Diethylstilbestrol, which caused inhibition at a dose of 10(-4) M, did not inhibit any enzyme leakage at any further concentrations of 10(-12) M to 10(-6) M. In the isolated plasma membrane of rat liver, Mg(2+)- and Na+,K(+)-adenosine triphosphatase activity was increased by E2 treatment at concentrations of 10(-6) M and 10(-4) M.
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PMID:Effect of estrogen on liver plasma membrane in rats. 147 13

We have compared the response of proton and water transport to oxytocin treatment in isolated frog skin and urinary bladder epithelia to provide further insights into the nature of water flow and H+ flux across individual apical and basolateral cell membranes. In isolated spontaneous sodium-transporting frog skin epithelia, lowering the pH of the apical solution from 7.4 to 6.4, 5.5, or 4.5 produced a fall in pHi in principal cells which was completely blocked by amiloride (50 microM), indicating that apical Na+ channels are permeable to protons. When sodium transport was blocked by amiloride, the H+ permeability of the apical membranes of principal cells was negligible but increased dramatically after treatment with antidiuretic hormone (ADH). In the latter condition, lowering the pH of the apical solution caused a voltage-dependent intracellular acidification, accompanied by membrane depolarization, and an increase in membrane conductance and transepithelial current. These effects were inhibited by adding Hg2+ (100 microM) or dicyclohexylcarbodiimide (DCCD, 10(-5) M) to the apical bath. Net titratable H+ flux across frog skin was increased from 30 +/- 8 to 115 +/- 18 neq.h-1.cm-2 (n = 8) after oxytocin treatment (at apical pH 5.5 and serosal pH 7.4) and was completely inhibited by DCCD (10(-5) M). The basolateral membranes of the principal cells in frog skin epithelium were found to be spontaneously permeable to H+ and passive electrogenic H+ transport across this membrane was not affected by oxytocin. Lowering the pH of the basolateral bathing solution (pHb) produced an intracellular acidification and membrane depolarization (and an increase in conductance when the normal dominant K+ conductance of this membrane was abolished by Ba2+ 1 mM). These effects of low pHb were blocked by micromolar concentrations of heavy metals (Zn2+, Ni2+, Co2+, Cd2+, and Hg2+). Lowering pHb in the presence of oxytocin (50 mU/ml) produced a transepithelial current (3 microA.cm-2 at pHb 5.5) which was blocked by 100 microM of Hg2+, Zn2+, or Ni2+ at the basolateral side, and by DCCD (10(-5) M) or Hg2+ (100 microM) from the apical side. The net hydroosmotic water flux (JH2O) induced by oxytocin in frog bladder sacs was blocked by inhibitors of H(+)-adenosine triphosphatase (ATPase). Diethylstilbestrol (DES 10(-5) M), oligomycin (10(-8) M), and DCCD (10(-5) M) prevented JH2O when present in the lumen. These effects cannot be attributed to inhibition of metabolism since cyanide (10(-4) M), or 2-deoxyglucose (10(-3) M) had no effect on JH2O.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Common channels for water and protons at apical and basolateral cell membranes of frog skin and urinary bladder epithelia. Effects of oxytocin, heavy metals, and inhibitors of H(+)-adenosine triphosphatase. 164 38

Homogeneous preparations of cytoplasmic membrane isolated from Staphylococcus aureus 6538P exhibited membrane-associated adenosine triphosphatase (ATPase) activity. Membrane ATPase activity was activated by divalent cations (4.0 mM: Mg2+ greater than Mn2+ greater than Co2+ greater than Zn2+), and ATP was hydrolyzed more readily than other nucleoside triphosphates and phosphorylated substrates. The pH optimum for the membrane ATPase was 6.5. The ATPase could not be released from the membrane by differential osmotic treatments, but detergent treatment effectively solubilized active enzyme. The nonionic detergent Triton X-100 (1%) released a protein with ATPase activity, after substrate-dependent staining in polyacrylamide gels, that differed slightly in electrophoretic migration when compared to the active enzyme solubilized with sodium dodecyl sulfate (0.1%). Membrane-associated ATPase activity was inhibited by N,N'-dicyclohexylcarbodiimide (0.001 to 1 mM) and NaF (50% inhibition at 5 mM NaF). Azide and trypsin inhibited activity, whereas ouabain had a slight inhibitory effect. Diethylstilbestrol showed appreciable activation of the membrane ATPase over the range employed (0.001 to 1 mM).
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PMID:Staphylococcus aureus adenosine triphosphatase: inhibitor sensitivity and release from membrane. 645 44

Estrogen status is known to affect the incidence of cardiovascular disease. Experiments were designed to prove the influences of in vivo estrogen manipulations on vascular hyperpolarization and relaxation mediated by endothelium-derived hyperpolarizing factor (EDHF), and to explore the possible mechanism contributing to the altered EDHF responses in estrogen-deficient states. Mesenteric arteries with intact endothelium were isolated from sham-operated (control), ovariectomized (OVX), or OVX with 17beta-estradiol replacement (OVX + E ) female rats. In the presence of apamin and charybdotoxin, there was no difference between groups in relaxations to the Ca ionophore A23187 and the endoplasmic reticulum Ca -adenosine triphosphatase inhibitor cyclopiazonic acid (CPA). However, N -nitro-L-arginine produced a marked decrease in A23187- and CPA-induced relaxations in OVX compared with control and OVX + E arteries. In control arteries, A23187 and CPA elicited membrane hyperpolarization in a sustained manner. In contrast, A23187 produced only a small and transient hyperpolarizing effect in OVX arteries. OVX also greatly attenuated the sustained pattern of hyperpolarization to CPA. Such changes in hyperpolarizations were not seen in OVX + E arteries. The EDHF-mediated relaxant and hyperpolarizing responses of control arteries to A23187 and CPA were significantly inhibited by the gap junction inhibitor 18 alpha-glycyrrhetinic acid. Immunohistochemical examination for connexin-43 showed that the expression was abundant along the endothelial layer in control and OVX + E arteries, while being much less in OVX arteries. It was concluded that estrogen deficiency specifically impairs EDHF-mediated vascular actions. This may be partly explained by the reduced expression of connexin-43, a protein molecule that could form myoendothelial gap junction channels.
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PMID:Ovariectomy attenuates hyperpolarization and relaxation mediated by endothelium-derived hyperpolarizing factor in female rat mesenteric artery: a concomitant decrease in connexin-43 expression. 1245 28