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)

Mercuric chloride (HgCl2), a neurotoxic compound, inhibited the adenosine triphosphatase (ATPase) system in a concentration-dependent manner. Hydrolysis of ATP was linear with time with or without HgCl2 in the reaction mixtures. Higher inhibition of (Na(+)-K+)ATPase activity by HgCl2 was observed in alkaline (8.0 to 9.0) pH and at lower temperatures (17 to 32 degrees). Activation energy values were increased slightly in the presence of HgCl2. Activation of (Na(+)-K+)ATPase by ATP in the presence of HgCl2 showed a decrease in Vmax from 15.29 to 5.0 mumol of inorganic phosphate (Pi)/mg protein/hr with no change in Km. Similarly, activation of K(+)-stimulated p-nitrophenyl phosphatase (K(+)-PNPPase) in the presence of HgCl2 showed a decrease in Vmax from 3.26 to 1.35 mumols of p-nitrophenol (PNP)/mg protein/hr with no change in Km. K(+)-activation kinetic studies indicated that HgCl2 decreased Vmax from 14.01 to 4.30 mumols Pi/mg protein/hr in the case of (Na(+)-K+)ATPase and from 3.45 to 2.40 mumols PNP/mg protein/hr in the case of K(+)-PNPPase with no changes in Km. Na(+)-activation of (Na(+)-K+)ATPase in the presence of HgCl2 showed a decrease in Vmax from 11.06 to 3.23 mumols Pi/mg protein/hr and an increase in Km from 1.06 to 2.08 mM. Preincubation of microsomes with sulfhydryl (SH) agents dithiothreitol, cysteine and glutathione protected HgCl2-inhibition of (Na(+)-K+)ATPase. The data suggest that HgCl2 inhibited (Na(+)-K+)ATPase by interfering with the dephosphorylation of the enzyme-phosphoryl complex.
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PMID:Effect of mercuric chloride on the kinetics of cationic and substrate activation of the rat brain microsomal ATPase system. 216 72

p-Aminohippurate (PAH) uptake by teased flounder renal tubules was concentrative, Na-dependent, dependent on aerobic metabolism and inhibited by competitor organic anions and ouabain. Dose-response data for ouabain inhibition of PAH transport and tubule Na,K-adenosine triphosphatase (ATPase) activity were identical. In ouabain-treated tubules, reductions in PAH uptake correlated with alterations in total tissue Na and K even though both were not affected during the first 5 to 10 min of ouabain exposure. No such delay was found with HgCl2 and, as with ouabain, reductions in transport correlated well with alterations in tissue Na and K. Tissue respiration data indicated that low concentrations of HgCl2 rapidly affected the Na,K-ATPase. With higher HgCl2 concentrations, intracellular metabolic sites appeared to be affected. Transport studies with ouabain-poisoned tubules and plasma membrane vesicles indicated that the energetically uncoupled PAH carrier(s) were affected by HgCl2, but carrier sensitivities to Hg were lower than for the Na,K-ATPase. The data indicate that HgCl2 inhibits PAH transport primarily by reducing ion gradients that drive PAH transport. Both inhibition of Na,K-ATPase and increases in membrane permeability to Na and K appear to be involved.
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PMID:Heavy metal inhibition of p-aminohippurate transport in flounder renal tissue: sites of HgCl2 action. 627 Mar 7

Mediated D-glucose and cycloleucine uptakes by killifish intestinal slices and everted sacs were reduced in a dose- and time-dependent manner by HgCl2 exposure, but nonmediated components of nutrient uptake were not affected. Transport processes in intestinal slices from sea water and fresh water-adapted fish exhibited identical sensitivities to HgCl2. The inhibitory effects of mucosal plus serosal exposure (slices) were no greater than the effects of mucosal exposure alone (sacs), indicating that primary inhibitory sites were on the brush border membrane of the tissue. One- to 5-min slice exposures (which caused substantial inhibition of nutrient transport) did not affect cellular water or electrolyte levels (indirect measures of Na,K-adenosine triphosphatase activity). With brush border membrane vesicles from killifish and flounder small intestine, HgCl2 affected only the Na-dependent component of D-glucose up-take. Vesicle Na permeability was not increased by HgCl2 exposure. Kinetic studies with killifish slices and flounder vesicles indicated that both Km and Vmax for glucose transport were affected by HgCl2. Taken together, these findings indicate that HgCl2 blocks intestinal nutrient transport by interacting directly with brush border membrane transport proteins; the kinetic data indicate that multiple sites on these proteins are probably affected.
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PMID:HgCl2 inhibition of nutrient transport in teleost fish small intestine. 745 9

Effects of oral administration of mercuric chloride (HgCl2, 1.25 mg/kg) daily for 30 d on the mouse testis, vas deferens, epididymis, and cauda epididymal sperm were investigated. Testis, vas deferens, and epididymis functions were evaluated with respect to sperm count, motility, and viability, and biochemical tests, including succinate dehydrogenase (SDH), adenosine triphosphatase, sialic acid, protein, cholesterol, and glycogen levels in these tissue. Sperm morphology and sperm nuclear integrity were evaluated with standard staining methods. Treatment did not affect whole body and tissue weights. Sperm parameters and fertility were reduced by HgCl2 and most of the biochemical parameters declined. Morphologic histologic alterations were also observed in the tissues studied. All parameters partially recovered after withdrawal of HgCl2 for 45 d.
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PMID:Reversible effects of mercuric chloride on reproductive organs of the male mouse. 891 13

Mercury intoxication has been associated with male reproductive toxicity in experimental animals and mercury may have the potential to produce adverse effects on fertility in men. Vitamin E may protect against toxic effects of mercury in the liver and other tissues. To investigate the protective role of vitamin E against mercuric chloride toxicity for the testis, epididymis, and vas deferens of adult male mice, animals were treated with either mercuric chloride 1.25 mg/kg/day, vitamin E 2 mg/kg/kg, or a combination of the two treatments. Control animals were treated with water. Treatments were administered by daily gavage for 45 days. An additional group of animals treated with mercuric chloride were permitted to recover for 45 days after mercuric chloride treatments. Parameters studied included serum testosterone, epididymal sperm count, motility, and morphology, epididymal and vas deferens adenosine triphosphatase (ATPase), phosphorylase, sialic acid, glycogen and protein, testicular succinate dehydrogenase (SDH), phosphatases, cholesterol, ascorbic acid, and glutathione. Fertility was evaluated by sperm positive vaginal smears after overnight cohabitation with a female. Mercuric chloride produced a reduction in epididymal sperm count, sperm motility, and sperm viability, and there were no sperm-positive smears in this group. Biochemical tests from the male reproductive organs were also altered by mercuric chloride treatment. Coadministration of vitamin E with mercuric chloride prevented the changes in sperm and biochemical parameters and was associated with control rates of sperm positive smears after cohabitation. Animals given vitamin E with mercuric chloride also had lower concentrations of mercury in the testis, epididimyis, and vas deferens. Permitting animals to recover for 45 days after mercuric chloride treatment resulted in partial recovery of sperm and biochemical parameters. Vitamin E cotreatment has a protective role against mercury-induced male reproductive toxicity.
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PMID:Protective effect of vitamin E against mercuric chloride reproductive toxicity in male mice. 1173 24