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PubMed1996

Neutron induced recoil protons of restricted energy and range and biological effectiveness.

Low energy neutrons (<2 MeV), those of principal concern in radiation protection, principally initiate recoil protons in biological tissues. The recoil protons from monoenergetic neutrons form rectangular distributions with energy. Monoenergetic neutrons of different energies (<2 MeV) will then produce overlapping recoil proton spectra. By overlapping the effects of individual deposition events, determined microdosimetrically for cell nuclear dimensions, from such neutron beams the biological effectiveness of recoil protons within defined energy and range bounds can be determined. Here chromosomal aberrations per cell have been quantified following irradiation of Vicia faba cells with monoenergetic neutrons of 230, 320, 430, and 1,910 keV. Aberration frequencies from cells from part of the cell cycle, thereby limiting nuclear dimensions, were linearly related to dose and to the frequency of proton recoils per nucleus. The 320 keV neutrons were the most biologically effective per unit absorbed dose and 430 keV neutrons most effective per recoil proton, with 21% of recoils inducing aberrations. After extraction of effectiveness per proton recoil within each energy and range bounds (0-230, 230-320, 320-430, and 430-1,910 keV), it was concluded that recoil protons with energies of about 200-300 keV, traveling 2.5-4 microm and depositing energy at about 80 keV micrometer(-1), are more efficient at aberration induction than those recoil protons of lesser range though near equivalent LET and those of greater range through lesser LET. This approach allows for assessment of the biological effectiveness of individual energy deposition events from low energy neutrons, the lowest dose a cell can receive, and provides an alternative to considerations of relative biological effectiveness.

Cell Cycle↗
PubMed1996

Effect of proton pump inhibitors on the detection of Helicobacter pylori in gastric biopsies.

BACKGROUND: Proton pump inhibitors are known to decrease the activity of Helicobacter pylori organisms within the stomach and to shift their distribution proximally. This effect may reduce the sensitivity of histological examination and rapid urease testing for H. pylori on biopsies taken from recommended sites. It is of particular relevance if a proton pump inhibitor has been prescribed before the patient has undergone diagnostic endoscopy. METHODS: We studied patients referred to our open-access upper gastrointestinal endoscopy service who had either been on no medication (controls) or were already taking proton pump inhibitors. Biopsies taken from the gastric antrum and corpus were used for rapid urease testing and for histological examination. Sera, taken from patients who had no evidence of H. pylori in biopsies, were tested for IgG H. pylori antibodies as an alternative indicator of infection. RESULTS: H. pylori organisms were detected by histological examination in 27 of 40 controls (68%) and in 13 of 25 patients taking proton pump inhibitors (52%). Among patients with positive histology (organisms detected in either antral or corpus biopsies, or both), only the sensitivity of the antral urease test read at 1 h was significantly lower in patients taking proton pump inhibitors than in controls, with no significant difference in sensitivities of the antral urease test at 24 h, of the corpus urease test at 1 or 24 h, or of histology from the antrum or corpus. Of patients with negative histology, none of 13 controls compared with six of 12 patients taking proton pump inhibitors (50%) had positive serology (P = 0.005). Five (83%) of the six histology-negative, seropositive patients taking proton pump inhibitors had histological changes consistent with H. pylori gastritis even though no organisms were detected. CONCLUSIONS: Treatment with a proton pump inhibitor before endoscopy reduces the sensitivity of antral and corpus biopsies for H. pylori detection, both by urease testing and histological examination. If proton pump inhibitors already prescribed cannot be discontinued for an adequate period before endoscopy, patients should have biopsies taken from the corpus as well as from the antrum, and serum should be tested for H. pylori.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2004

Systematic review: Is there excessive use of proton pump inhibitors in gastro-oesophageal reflux disease?

BACKGROUND: Proton-pump inhibitors are often recommended for continuous use in gastro-oesophageal reflux disease, but this may not be necessary in all patients. AIM: To ascertain the level of evidence for alternative strategies for proton-pump inhibitor treatment in gastro-oesophageal reflux disease. METHODS: We searched for observational or interventional studies examining alternatives to continuous proton-pump inhibitor treatment in gastro-oesophageal reflux disease. RESULTS: Non-randomized studies suggest that some patients with gastro-oesophageal reflux disease, including some with erosive oesophagitis, may be adequately maintained on proton-pump inhibitor therapy given less frequently than once daily. However, the results may not be generalizable. Four high quality randomized-controlled trials compared 'on-demand' proton-pump inhibitor and placebo treatment in endoscopy-negative reflux disease; all found this effective for most patients. One high quality randomized-controlled trial found intermittent courses of a proton-pump inhibitor or H2-receptor antagonist in erosive oesophagitis or endoscopy-negative reflux disease adequate for almost half of the patients studied. Up to 80% of patients on continuous high-dose proton-pump inhibitor treatment for gastro-oesophageal reflux disease can be 'stepped down' to less intensive therapy. CONCLUSIONS: On-demand proton-pump inhibitor treatment may be appropriate in endoscopy-negative reflux disease. In gastro-oesophageal reflux disease, patients taking more than once daily or high-dose proton-pump inhibitor treatment, a step down to once daily or standard dose therapy should be attempted.

Adolescent↗
PubMed2005

Systematic review and meta-analysis: is 1-week proton pump inhibitor-based triple therapy sufficient to heal peptic ulcer?

AIMS: To systematically review the efficacy on ulcer healing of 1-week combination of a proton pump inhibitor plus two antibiotics and to perform a meta-analysis of randomized clinical trials to evaluate whether 7 days of proton pump inhibitor-based triple therapy is sufficient to heal peptic ulcer. METHODS: Studies where 1-week proton pump inhibitor-based triple therapy was administered to heal peptic ulcer were included. Randomized clinical trials comparing the efficacy on ulcer healing of 7-day proton pump inhibitor-based triple therapy versus this same regimen but prolonging the proton pump inhibitor for several more weeks were included in the meta-analysis. Electronic and manual bibliographical searches were conducted. Meta-analysis was performed combining the odds ratios of the individual studies. RESULTS: Twenty-four studies (2342 patients) assessed ulcer healing with 1-week proton pump inhibitor-based triple therapy. Mean healing rate was 86%, and 95% in Helicobacter pylori-eradicated patients. Six studies (862 patients), were included in the meta-analysis. Mean ulcer healing rate with a 7-day treatment was 91% versus 92% when proton pump inhibitor was prolonged for 2-4 more weeks (odds ratio = 1.11; 95% confidence interval = 0.71-1.74). CONCLUSION: In patients with peptic ulcer and H. pylori infection, prolonging therapy with proton pump inhibitor after a triple therapy for 7 days with a proton pump inhibitor and two antibiotics is not necessary to induce ulcer healing.

Anti-Bacterial Agents↗
PubMed2006

Persistence and adherence to proton pump inhibitors in daily clinical practice.

BACKGROUND: Proton pump inhibitors are widely used, but little is known about the usage pattern in different indications. AIM: To analyse proton pump inhibitor usage patterns in the general population. METHODS: A cohort of 16 311 incident proton pump inhibitor users was identified in the Integrated Primary Care Information database, a Dutch general practice research database. Persistence and adherence were calculated by indication. Risk factors were identified by logistic regression analysis. RESULTS: One-year persistence was 31% in patients using proton pump inhibitors for gastro-oesophageal reflux. Persistence was higher in oesophagitis grade A/B (54%), grade C/D (73%) and Barrett's oesophagus (72%), compared to patients with only reflux symptoms (27%). Approximately 25% of patients with non-reflux dyspepsia or Helicobacter pylori-associated indications used proton pump inhibitors for more than 6 months. Half of all patients used proton pump inhibitors <80% of time indicating intermittent use, which was independent of indication. Exception were patients with Barrett's oesophagus, who were most adherent. CONCLUSIONS: A substantial proportion of patients with indications not requiring long-term treatment use proton pump inhibitors for an extended period. Half of the patients used proton pump inhibitors on-demand or intermittently. Such usage pattern is probably sufficient for most patients, but may be inadequate if proton pump inhibitors are used for serious diseases, such as severe oesophagitis or Barrett's oesophagus.

Adult↗
PubMed1997

Mutation of arginine 134 to lysine alters the pK(a)s of key groups involved in proton pumping by bacteriorhodopsin.

Arginine 134 is located near the extracellular surface of bacteriorhodopsin (bR) and may interact with one or more nearby glutamate residues. In the bR mutant R134K, light-induced Schiff-base deprotonation (formation of the M intermediate) exhibits several kinetic components and has a complex pH dependence. The kinetics and pH dependence of M formation were analyzed using the following general guidelines for interpreting M formation: (1) The fastest component of M formation reflects the redistribution of the Schiff-base proton to D85, the usual proton acceptor, in response to the change in the proton affinities of the Schiff base and D85 early in the photocycle; (2) Two additional components of M formation reflect transitions between spectroscopically similar substates of M. By applying these guidelines, supplemented by information about the pK(a)s of D85 and the proton release group from acid (purple-to-blue) and alkaline titrations of the absorption spectra of the unphotolyzed R134K pigment, we explain the pH dependence of M formation as being due to titration of the counterion, D85, and of the proton release group. We calculate, in R134K, that the pKa of D85 is 4.6 in the unphotolyzed state, while the pKa of the proton release group is 8.0 in the unphotolyzed state but drops to approximately 5.8 in the M intermediate. The same value for the pKa of the proton release group in the M intermediate is obtained when we use photocurrent measurements to monitor proton release. The altered values of these pK(a)s relative to the corresponding values in wild-type bR suggest that D85 and the proton release group are coupled more weakly in R134K than in the wild type.

Arginine↗
PubMed2003

Differences in conductance of M2 proton channels of two influenza viruses at low and high pH.

The M2 protein of influenza A viruses forms a proton channel involved in modifying virion and trans Golgi pH during infection. Previous studies of the proton current using whole-cell patch clamp of mouse erythroleukaemia (MEL) cells expressing the M2 protein of the "Weybridge" strain provided evidence for two protonation sites, one involved in permeation, the other in activation by acid pH. The present report compares the M2 channels of two different strains of influenza virus, "Weybridge" (WM2) and "Rostock" (RM2). Whereas with external acid pH the current-voltage relations showed similar small degrees of inward rectification, a similar apparent K(d) of approximately 10 microM for proton permeation and a high selectivity for protons over Na(+), the two M2 proteins differed in whole-cell conductance at low and high pH. The proton conductance of unit membrane area was on average 7-fold greater in RM2- than WM2-expressing MEL cells. At high external pH WM2 was shown previously to have small conductance for outward current at positive driving potential. In contrast, RM2 shows high conductance for outward current with high external pH, but shows small conductance for inward current with high internal pH, conditions in which WM2 shows high conductance for inward current. The different properties of the conductances due to the two channels at high pH were determined by three amino acids in their transmembrane domains. All intermediate mutants possessed one or other property and transformation of the WM2 phenotype into that of RM2 required substitution in all three residues V27I, F38L and D44N; single substitutions in RM2 effected the opposite phenotypic change. The significance of this difference for virus replication is not clear and it may be that the higher proton flux associated with RM2 is the main factor determining its increased ability to dissipate pH gradients. It is apparent, however, from the specific differences in the sidedness of the pH-induced changes in voltage dependence of the whole-cell current that this is an intrinsic property of the virus proton channel which may have parallels with regulation of other proton channels.

Animals↗
PubMed2005

Distributions of beta+ decayed nuclei generated in the CH2 and H2O targets by the target nuclear fragment reaction using therapeutic MONO and SOBP proton beam.

In proton radiotherapy, the irradiation dose can be concentrated on a tumor. To use this radiotherapy efficiently in the clinical field, it is necessary to evaluate the proton-irradiated area and condition. The proton-irradiated area can be confirmed by coincidence detection of pair annihilation gamma rays from beta+ decayed nuclei generated by target nuclear fragment reaction of irradiated proton nuclei and nuclei in the irradiation target. In this study, we performed experiments of proton irradiation to a polyethylene (PE:CH2) target containing 12C nuclei, which is a major component of the human body, and a gelatinous water (H2O) target containing 16O nuclei at different proton irradiation energy levels under different beam conditions of mono-energetic Bragg peak and spread-out Bragg peak. The distribution of the activity in the target after proton irradiation was measured by a positron emission tomography (PET) apparatus, and compared with the calculated distribution. The temporal dependence of the activity distribution during the period between the completion of proton irradiation and the start of measurement by the PET apparatus was examined. The activity by clinical proton irradiation was 3 kB/cc in the PE target and 13 kB/cc in the water target, indicating that the intensity was sufficient for the evaluation of the distribution. The range of the activity distribution against the physical range was short (several millimeter water equivalent length), indicating the presence of target dependence. The range difference in the water target was slightly large with time dependence until the start of measurement. The difference of the lateral widths with full width half at maximum in the distributions of the measured irradiated dose and activity was within 1 mm.

Algorithms↗
PubMed1997

Gastric mucus of the guinea pig: proton carrier and diffusion barrier.

Proton transport with the gastric mucus was investigated in the guinea pig in vitro by use of three experimental series. In series I, pH profiles were obtained in the mucus and mucosa of a gastric explant with fine-tipped double-barreled microelectrodes. With a luminal pH of 1.8, pH increased across this layer to approximately 6 at the epithelial surface. Thickness of the gastric mucous gel layer increased continuously by 170 +/- 100 microns/h in the unstimulated and by 450 +/- 120 microns/h in the histamine-stimulated preparation (means +/- SD). In series II, fresh guinea pig gastric mucus was obtained from the gastric mucosa and titrated at 10 degrees C from pH 6.5 to 0.7, followed by an incubation period of 30 min at 37 degrees C. During this incubation period, a spontaneous acidic shift was observed, corresponding to a proton release from the mucus of 130 +/- 19 mM. This proton release could be blocked by the pepsin inhibitor pepstatin and was not observed when titrating down to only pH 3. Buffer values calculated as the mean slope of the titration curves in the pH range of 7 to 3 averaged 40 mM/pH unit. In series III, when titration was repeated with purified porcine mucin, no proton release was observed during incubation at pH 1.0, unless pepsinogen (375 U/ml) had been added before titration. Proton release during incubation at pH 1.0 and 37 degrees C in the presence of pepsinogen averaged 50 mM. The data suggest that protons secreted by the gastric mucosa are buffered by the continuously secreted mucus and transported, bound to the proteins of the mucus, toward the gastric lumen. During this transport, pepsinogen is converted within the mucus to pepsin. Pepsin modifies the buffering properties of the mucus, whereby protons are released from the protein binding. Thus the mucus forms a vehicle for proton transport toward the gastric lumen while, at the same time, constituting a diffusion barrier to prevent proton backdiffusion toward the gastric epithelium.

Animals↗
PubMed1981

Extracellular proton release by stimulated neutrophils.

We have tried to elucidate the mechanism of phagosome acidification in human neutrophils. Assuming that phenomena occurring at the plasma membrane reflect reactions in the phagocytic vacuoles, we have stimulated human neutrophils with agents that induce a "respiratory burst," and we have measured the release of protons into the extracellular medium. Phorbol myristate acetate, N-formyl-methionyl-leucyl-phenylalanine and serum-opsonized zymosan particles each caused a rapid release of protons, concomitant with the increase in oxygen consumption. The stimulated release of protons was strictly coupled to the increase respiration of the cells, because inhibition of the respiration of either anaerobiosis, chlorpromazine, or glycolytic inhibitors also inhibited the release of protons. Also, in the presence of the above-mentioned stimulating agents, neutrophils from three patients with chronic granulomatous disease enhanced neither respiration not proton release. In normal cells, the ratio of deltaH+/-deltaO2 was 1.04 +/- 0.19 (mean +/ SD, n = 13). The mechanism of this proton release is not clear. The amount of lactic and carbonic acid produced by stimulated neutrophils was inadequate to explain the amount of protons released. Perhydroxyl radicals were also ruled out as the source of the protons. Because the cells did not release measurable amounts of phosphate ions, a phosphate-hydroxyl-ion antiport was also excluded. Finally, the lack of any effect of uncouplers renders it unlikely that a respiration-driven proton gradient is built up across the plasma membrane.

Granulomatous Disease, Chronic↗
PubMed2000

The effect of metabolic depression on proton leak rate in mitochondria from hibernating frogs.

Futile cycling of protons across the mitochondrial inner membrane accounts for 20 % or more of the total standard metabolic rate of a rat. Approximately 15 % of this total is due to proton leakage inside the skeletal muscle alone. This study examined whether the rate of proton leak is down-regulated as a part of a coordinated response to energy conservation during metabolic depression in cold-submerged frogs. We compared the proton leak rate of skeletal muscle mitochondria isolated from frogs at different stages of hibernation (control, 1 month and 4 months of submergence in normoxia and hypoxia). The kinetics of mitochondrial proton leak rate was unaltered throughout normoxic and hypoxic submergence. The state 4 respiration rates did not differ between control animals and frogs hibernating in normoxia. In contrast, the state 4 respiration rates obtained from frogs submerged in hypoxic water for 4 months were half those of control animals. This 50 % reduction in respiration rate in hypoxic hibernation was due to a reduction in electron transport chain activity and consequent decrease in mitochondrial membrane potential. We conclude that proton leak rate is reduced during metabolic depression as a secondary result of a decrease in electron transport chain activity, but that the proton conductance is unchanged. In addition, we show that the rate of proton leakage and the activity of the electron transport chain are lower in frogs than in rats, strengthening the observation that mitochondria from ectotherms have a lower proton conductance than mitochondria from endotherms.

Animals↗
PubMed2004

Simulation of proton neutralization effect for neutron dosimetry.

Neutron dose is transferred to biological materials through the recoil protons produced by elastic scattering. When a low-velocity proton collides with the atoms or molecules of a target, it changes to a hydrogen atom by electron capture; this hydrogen atom then changes to a proton by losing the electron. Because the hydrogen atom has a different ionization cross section from that of a proton, the charge exchange processes need to be considered to calculate stopping power for low energy protons. The proton neutralization effect has been simulated by using a proton track structure code developed by taking into account charge exchange processes. The microdosimetric spectrum for 1 MeV neutrons was calculated by assuming a continuous slowing down approximation (csda) and the results of the proton track code. It was found that hydrogen atoms after proton neutralized by electron capture contribute about 24% to neutron dose.

Computer Simulation↗
PubMed2000

Correlation of two levels of space proton flux with monthly distribution of deaths from cardiovascular disease and suicide.

In our previous studies /1-3/ we described some significant links between monthly number of deaths due to cardiovascular disease and suicide and space proton flux > 90 MeV. The aims of the present study were to compare the relationship of some solar and geomagnetic parameters with space proton fluxes of > 60 and > 90 MeV; to examine the monthly correlation of these two proton groups with the monthly death distribution in two countries, Israel and Lithuania. Physical data were obtained from the National Geophysical Data Center and the SESC in Boulder, CO; NSSDC in Goddard Space Flight Center, USA, and the Izmiran Institute of the Academy of Sciences in Russia. Pearson correlation coefficients and probabilities were compared for 56-180 consecutive months. Proton flux of > 60 MeV significantly correlated with three of the four studied monthly geomagnetic activity indices (Ap, Am, Dst), but not with such solar activity markers as sunspot number and solar flux (2800 MGH, 10.6 cm). There was no significant relationship between proton flux of > 60 MeV and monthly number of deaths from cardiovascular diseases and suicide, in contrast to the results for > 90 MeV. From the data available during the 36 months (1986-1988), there was no correlation between monthly levels of > 60 to > 90 MeV. In conclusion, a monthly space proton flux of > 60 MeV is not significantly correlated with the monthly death distribution from cardiovascular disease and suicide and some solar activity indices, such as proton flux of > 90 MeV. It is possible that the 60-90 MeV fraction in the > 60 MeV proton flux "blunts" the cosmobiological relationship between proton flux of > 90 MeV and monthly death number.

Cardiovascular Diseases↗
PubMedDate not supplied

Proton uptake by light induced interaction between rhodopsin and G-protein.

The light-induced proton uptake of rod outer segment disc membranes has been investigated in the absence and presence of G-protein. Proton uptake was measured as the alkalisation of the suspending medium using a pH electrode and/or the indicator dye bromocresol purple. It was found that besides the known proton uptake of photolysed rhodopsin additional uptake of one proton accompanies formation of the complex between rhodopsin and G-protein. No measurable proton uptake was found under conditions of rapid redissociation of the complex indicating an only transient protonation during its lifetime. Proton uptake was the same in washed membranes recombined with G-protein and in ordinarily stacked rod outer segments. The additional proton uptake reported here is not due to enhanced formation of the protonated photoproduct metarhodopsin II.

Animals↗
PubMed2005

Protons trap NR1/NR2B NMDA receptors in a nonconducting state.

NMDA receptors are highly expressed in the CNS and are involved in excitatory synaptic transmission, as well as synaptic plasticity. Given that overstimulation of NMDA receptors can cause cell death, it is not surprising that these channels are under tight control by a series of inhibitory extracellular ions, including zinc, magnesium, and H+. We studied the inhibition by extracellular protons of recombinant NMDA receptor NR1/NR2B single-channel and macroscopic responses in transiently transfected human embryonic kidney HEK 293 cells using patch-clamp techniques. We report that proton inhibition proceeds identically in the absence or presence of agonist, which rules out the possibility that protonation inhibits receptors by altering coagonist binding. The response of macroscopic currents in excised patches to rapid jumps in pH was used to estimate the microscopic association and dissociation rates for protons, which were 1.4 x 10(9) m(-1) sec(-1) and 110-196 sec(-1), respectively (K(d) corresponds to pH 7.2). Protons reduce the open probability without altering the time course of desensitization or deactivation. Protons appear to slow at least one time constant describing the intra-activation shut-time histogram and modestly reduce channel open time, which we interpret to reflect a reduction in the overall channel activation rate and possible proton-induced termination of openings. This is consistent with a modest proton-dependent slowing of the macroscopic response rise time. From these data, we propose a physical model of proton inhibition that can describe macroscopic and single-channel properties of NMDA receptor function over a range of pH values.

Animals↗
PubMed1995

Triiodothyronine-induced changes in proton efflux from rat skeletal muscle in vivo.

Hyperthyroidism is associated with muscle weakness, abnormal aerobic metabolism and increased lactate production. Muscle cell acidification during exercise is reduced, suggesting abnormally increased proton efflux. Using 31P magnetic resonance spectroscopy to measure cell pH and phosphocreatine concentration, we quantified effective proton efflux from rat leg muscle in vivo following 10-Hz sciatic nerve stimulation in seven rats injected with triiodothyronine (T3) for 5 days and in 11 controls. Proton efflux during recovery was sigmoidally pH-dependent in both groups but the initial proton efflux rate did not differ (16 +/- 3 mmol.kg-1.min-1 in treated animals vs 15 +/- mmol.kg-1.min.-1 in controls), despite significantly smaller pH change from basal in treated animals (0.60 +/- 0.04 vs 0.78 +/- 0.03 in controls, p = 0.002). The pH dependence of proton efflux can be characterized by an apparent Km, defined as the pH below basal at which proton efflux rate falls to half its start-of-recovery value. This Km was smaller in the T3-treated group (0.44 +/- 0.04 vs 0.59 +/- 0.03 in controls, p = 0.02). This suggests an increased affinity for protons by cell membrane proton transport processes such as the sodium-proton antiporter and may explain some of the metabolic changes seen clinically in hyperthyroid skeletal muscle.

Animals↗
PubMed1991

Colchicine-induced redistribution of proton pumps in kidney epithelial cells.

In kidney medulla, intercalated cells (ICs) all have an apical proton-pumping ATPase, but in the cortex, ICs with apical (type A cells) and basolateral (type B cells) proton pumps coexist. Proton pumps in proximal-tubule epithelial cells are located in a band of apical membrane at the base of the brush border. To determine the effect of microtubule disruption on proton-pump polarity in these cell types, we immunolocalized proton pumps in normal and colchicine-treated rat kidneys. In addition, NEM-sensitive ATPase was measured in brush-border (BBMV) and basolateral membrane vesicles from kidney cortex. Rats were injected with colchicine, and kidneys were fixed 4-24 h later. In both cortical and medullary IC, proton pumps were localized on vesicles that were scattered throughout the cell. A- and B-type ICs were no longer distinguishable on the basis of proton-pump polarity. In the medulla, no concentration of proton pumps at the basolateral pole of ICs was detectable. In proximal tubules, pumps were also scattered on vesicles throughout the cytoplasm. NEM-sensitive ATPase was reduced by over 60% in BBMV, and was also reduced in basolateral membranes, indicating no increased insertion of NEM-sensitive ATPase into basolateral membranes after colchicine treatment. We conclude that a change in the polymerization state of microtubules is not sufficient to account for the differential targetting of proton pumps in subpopulations of intercalated cells.

Adenosine Triphosphatases↗
PubMed1989

A vacuolar-type proton pump in a vesicle fraction enriched with potassium transporting plasma membranes from tobacco hornworm midgut.

Mg-ATP dependent electrogenic proton transport, monitored with fluorescent acridine orange, 9-aminoacridine, and oxonol V, was investigated in a fraction enriched with potassium transporting goblet cell apical membranes of Manduca sexta larval midgut. Proton transport and the ATPase activity from the goblet cell apical membrane exhibited similar substrate specificity and inhibitor sensitivity. ATP and GTP were far better substrates than UTP, CTP, ADP, and AMP. Azide and vanadate did not inhibit proton transport, whereas 100 microM N,N'-dicyclohexylcarbodiimide and 30 microM N-ethylmaleimide were inhibitors. The pH gradient generated by ATP and limiting its hydrolysis was 2-3 pH units. Unlike the ATPase activity, proton transport was not stimulated by KCl. In the presence of 20 mM KCl, a proton gradient could not be developed or was dissipated. Monovalent cations counteracted the proton gradient in an order of efficacy like that for stimulation of the membrane-bound ATPase activity: K+ = Rb+ much greater than Li+ greater than Na+ greater than choline (chloride salts). Like proton transport, the generation of an ATP dependent and azide- and vanadate-insensitive membrane potential (vesicle interior positive) was prevented largely by 100 microM N,N'-dicyclohexylcarbodiimide and 30 microM N-ethylmaleimide. Unlike proton transport, the membrane potential was not affected by 20 mM KCl. In the presence of 150 mM choline chloride, the generation of a membrane potential was suppressed, whereas the pH gradient increased 40%, indicating an anion conductance in the vesicle membrane. Altogether, the results led to the following new hypothesis of electrogenic potassium transport in the lepidopteran midgut. A vacuolar-type electrogenic ATPase pumps protons across the apical membrane of the goblet cell, thus energizing electroneutral proton/potassium antiport. The result is a net active and electrogenic potassium flux.

Adenosine Triphosphatases↗