ATPase Activity In Patients Research Articles

The effect of erythropoietin application on erythrocyte Na,K- ATPase activities in patients with diabetic polyneuropathy

Objectives: In this study we aimed to investigate the effects of erythropoietin administration on Na,K-ATPase enzyme activity in diabetic patients with polyneuropathy. Methods: The study was carried out at Meram Education and Research Hospital department of Nephrology and Selcuk University Meram School of Medicine Hospital department of Biochemistry, Turkey. Eleven diabetic patients with diabetic polyneuropathy and on erythropoietin therapy and ten healthy control were contributed to this study. Diabetic group was formed from the patients with polyneuropathy and on erythropoietin therapy. Erythropoietin was administered with a dose of 150 U/kg/ week to the patients. Heparinized blood samples were taken from the control group for once and from the patients for twice before and one month after the erythropoietin therapy. Erythrocyte membranes were isolated and erythrocyte membrane Na,K-ATPase enzyme activities were measured. Na,K-ATPase activities were given as mmolPi.mg.protein –1.10 min-1. Results: Na,K-ATPase enzyme activities were 2.91±0.38 μmolPi.mg.prt-1.10min-1, 1.93±0.38 μmolPi.mg.prt-1.10min-1 and 2.40±0.63 μmolPi.mg.prt-1.10min-1 in control group, and patient group before and after therapy, respectively. Na,K-ATPase enzyme activities decreased in patient group before the therapy compared to the control group and significantly increased in patient group after erythropoietin therapy compared to the basal levels of the patients. We determined 24% increase in erythrocyte Na,K-ATPase activities after one month EPO application compared to the basal levels. Conclusion: It was concluded that erythropoietin therapy could improve neuropathy and this improvement was supported with the increase in Na,K-ATPase activities which could be used as a marker.

Lecithin: Cholesterol Acyltransferase and Na+-K+-ATPase Activity in Patients with Breast Cancer

PurposeThe aim of this study was to determine whether plasma lecithin:cholesterol acyltransferase (pLCAT) and erythrocyte membrane Na+-K+-ATPase ase (emNaKATPs) activity have a correlation in breast cancer. This study compared these parameters at time points before and after treatment with radiotherapy.MethodsThe levels of pLCAT and emNaKATPs were assessed in 30 patients with breast carcinoma and 20 control subjects. While emNaKATPs was measured with spectrophotometric method, pLCAT levels was measured using a specific enzyme-linked immunosorbent assay.ResultspLCAT levels, both before and after radiotherapy, were found to be decreased in breast cancer patients than in the controls groups (p<0.001 and p<0.001, respectively). Also, pLCAT levels after radiotherapy were found to be decreased in breast cancer patients than the pLCAT levels before radiotherapy (p<0.001). The emNaKATPs activity were higher in the control group than in the breast cancer patients before/after radiotherapy (RT) (p<0.001 and p<0.001, respectively). At the same time, emNaKATPs activity before RT was higher in the breast cancer patients than emNaKATPs activity after RT (p<0.001). There was a significant correlation between pLCAT and emNaKATPs activity in breast cancer patients receiving radiotherapy (r=0.63, p<0.001), but no correlation between in breast cancer patients before RT and control group (r=0.023, p>0.05).ConclusionThe results of the present study demonstrated that decreased pLCAT and emNaKATPs activity levels in breast cancer patients after/before RT than control group. In addition, decreased emNaKATPs activity in breast cancer patients receiving radiotherapy may be due to decreased pLCAT concentrations and RT beam. In our opinion, altered activities of pLCAT and emNaKATPs are linked to the treatment effect of radiotherapy. These data may clarify the development of cell membrane dysfunction and lipid metabolism in breast cancer patients receiving radiotherapy.

Erythrocyte membrane Na+,K+-ATPase and Mg2+-ATPase activities in subjects with methylenetetrahydrofolate reductase (MTHFR) 677 C→T genotype and moderate hyperhomocysteinaemia. The role of L-phenylalanine and L-alanine

Increased homocysteine (Hcy) blood levels are correlated with vascular and neurological problems. The aim of our study was to investigate erythrocyte membrane Na(+),K(+)-ATPase and Mg(2+)-ATPase activities in patients with methylenetetrahydrofolate reductase (MTHFR) 677 C-->T genotype. Blood was obtained from 25 patients before and after folic acid supplementation and from controls (n=30) once. Plasma folate, vitamin B(12) and total antioxidant status (TAS) were measured using commercial kits, Hcy was determined by HPLC and membrane enzyme activities were measured spectrophotometrically. Mg(2+)-ATPase remained unaltered. Membrane Na(+),K(+)-ATPase activity was remarkably increased in patients (0.77+/-0.06 micromol Pi/h x mg protein) and decreased to normal levels (0.52+/-0.05 micromol Pi/h x mg protein; p<0.001) after therapy. TAS did not differ significantly before and after treatment. Hcy levels were significantly higher before therapy (25.4+/-2.8 micromol/L) than levels after therapy (12.1+/-2.0 micromol/L; p<0.001) and in controls (10.5+/-2.5 micromol/L, p<0.001). In vitro, L-phenylalanine (Phe) reversed to normal the stimulated enzyme from patients before therapy. In addition, Phe incubation of the Hcy activated membrane Na(+),K(+)-ATPase from controls resulted in restoration of its activity, whereas L-alanine (Ala) incubation protected the enzyme from Hcy activation. The increased membrane Na(+),K(+)-ATPase activity may be due to high -SH group Hcy levels. In vitro, Phe reversed the increase in enzyme activity induced by Hcy in controls, as well as the stimulated membrane enzyme in untreated patients. Ala protected the enzyme from Hcy action.

Erythrocyte membrane acetylcholinesterase, Na+, K+‐ATPase and Mg2+‐ATPase activities in patients with classical galactosaemia

Classical galactosaemia is commonly presented by high blood galactose (Gal) and galactose-1-phosphate (Gal-1-P) levels followed by mental retardation, seizures, etc. dependent on the mutation of the patients. To evaluate Gal and Gal-1-P in the blood of patients and to correlate their levels with their erythrocyte membrane acetylcholinesterase (AChE), Na+,K+-ATPase and Mg2+-ATPase activities. Blood was obtained from nine patients on poor diet (group B) followed by a 30-d strict diet (group A) and controls (group C) in order to evaluate Gal and Gal-1-P in Guthrie cards and to correlate their concentrations with the above enzyme activities, which were measured spectrophotometrically. With the patients on a "loose" diet, AChE, Na+,K+-ATPase and Mg2+-ATPase activities were found to be decreased, as compared with those on strict diet and controls. Significantly (p<0.01) inverse correlation coefficients of the enzyme activities were found with Gal-1-P levels. (a) AChE, Na+,K+-ATPase and Mg2+-ATPase activities were determined to be decreased in poorly controlled patients with classical galactosaemia. (b) The enzyme activities were inversely correlated with the Gal-1-P blood levels. (c) Since Na+,K+-ATPase in the erythrocyte membranes is the isomer of Na+,K+-ATPase distributed in many tissues and in the brain, evaluation of the enzyme activity in the erythrocytes could be a useful peripheral marker of Gal-1-P toxicity.

Direct measurement of gastric H+/K+-ATPase activities in patients with or withoutHelicobacter pylori-associated chronic gastritis

The role of Helicobacter pylori (H pylori) infection in gastric acid secretion of patients with chronic gastritis remains controversial. This study was designed to elucidate the effect of H pylori on H+/K+-ATPase activities in gastric biopsy specimens. Eighty-two patients with chronic gastritis who had undergone upper endoscopy were included in this study. H pylori infection was confirmed by rapid urease test and histology. Gastric H+/K+-ATPase activities and serum gastrin concentrations were measured by an enzymatic method and radioimmunoassay, respectively. For those patients who received triple therapy for eradicating H pylori, changes in the activity of gastric H+/K+-ATPase and serum gastrin levels were also measured. The mean gastric H+/K+-ATPase activity in H pylori-positive group (42 patients) was slightly higher than that in H pylori-negative group (29 patients) (169.65+/-52.9 and 161.38+/-43.85 nmol Pi/(mg.h), respectively, P=0.301). After eradication of H pylori, the gastric H+/K+-ATPase activities slightly decreased compared to prior therapy (165.03+/-59.50 and 158.42+/-38.93 nmol Pi/(mg.h), respectively, P=0.805). The mean basal gastrin concentration was slightly higher in H pylori-positive patients than in H pylori-negative patients (87.92+/-39.65 pg/mL vs 75.04+/-42.57 pg/mL, P=0.228). The gastrin levels fell significantly after the eradication of H pylori. (Before treatment 87.00+/-30.78 pg/mL, after treatment 64.73+/-18.96 pg/mL, P=0.015). Gastric H+/K+-ATPase activities are not associated with H pylori status in patients with chronic gastritis.

Serum E-selectin and erythrocyte membrane Na+K+ ATPase levels in patients with rheumatoid arthritis

We conducted this study to assess serum soluble E-selectin (sE-selectin) levels and erythrocyte membrane Na(+)K(+) ATPase activity in patients with rheumatoid arthritis (RA) and correlate the levels with disease activity. Levels of sE-selectin were measured in the serum of 20 patients with RA and 20 control subjects by an enzyme-linked immunosorbant assay. Na(+)K(+) ATPase activity was determined by a colorimetric method in RA patients and healthy controls. There were no statistically significant differences between the two groups with respect to demographic data such as age and sex (p > 0.05). The serum levels of sE-selectin, ESR and C-reactive protein (CRP) in RA patients were significantly higher than in healthy controls (p < 0.001). Erythrocyte membrane Na(+)K(+) ATPase activity was significantly lower in the RA group than in the control group (p < 0.001). Correlation analysis revealed significant positive correlations between soluble E-selectin and ESR (r = 0.457; p < 0.05) and CRP (r = 0.682; p < 0.01) levels. There were statistically significant negative correlations between erythrocyte membrane Na(+)K(+) ATPase activity and ESR (r = -0.450; p < 0.05) and CRP (r = -0.446; p < 0.05) levels. Additionally, a significant negative correlations between sE-selectin and Na(+)K(+) ATPase activity was observed (r = -0.80; p < 0.001). These results show that decreases in erythrocyte membrane Na(+)K(+) ATPase activity and increases in sE-selectin are observed in RA, and that increased levels of sE-selectin may also reflect disease status or activity.

The effect of diet on total antioxidant status, erythrocyte membrane Na+,K+-ATPase and Mg2+-ATPase activities in patients with classical galactosaemia

Classical galactosaemia is characterized by high levels of galactose-1-phosphate (Gal-1-P), galactose and galactitol. In vitro studies have shown modulation of the rat brain Na+,K+-ATPase and Mg2+-ATPase activities by Gal-1-P. The aim of this study was to evaluate the erythrocyte membrane Na+,K+-ATPase and Mg2+-ATPase activities in galactosaemic patients and to correlate them to Gal-1-P, total antioxidant status (TAS) and membrane protein content (PC). Nine patients (N=9) originally on "loose diet" (group B) were requested to follow their diet strictly (group A). Twelve healthy children were the controls (group C). The activities of the enzymes, TAS and Gal-1-P in blood were determined spectrophotometrically. In the in vitro study, erythrocyte membranes from controls were preincubated with Gal-1-P (300 microM), and then with l-cysteine (0.83 mM) or reduced glutathione (0.83 mM) whereas these from the patients with the antioxidants only. Na+,K+-ATPase, Mg2+-ATPase, TAS and PC were significantly (P<0.001) reduced (0.31+/-0.03, 1.7+/-0.2 micromol Pi/hxmg protein, 0.89+/-0.02 mmol/l, 36.8+/-2.0 g/l, respectively) in group B as compared with those of group A (0.58+/-0.06, 2.5+/-0.2 micromol Pi/hxmg protein, 1.41+/-0.11 mmol/l, 51.5+/-3.1g/l, respectively) and controls (0.67+/-0.05, 3.2+/-0.2 micromol Pi/hxmg protein, 1.65+/-0.12 mmol/l, 64.0+/-3.5 g/l, respectively). Gal-1-P levels in group B was significantly higher than those in group A and controls. Positive correlation coefficients were found between the enzyme activities, PC and TAS whereas Gal-1-P inversely correlated to the enzyme activities. Incubation of the erythrocyte membranes from the patients with the antioxidants failed to restore the activities of inhibited enzymes, whereas the inhibition by Gal-1-P in controls was reversed. High blood Gal-1-P concentrations resulted in low TAS and PC. The inhibition of Na+,K+-ATPase and Mg2+-ATPase may be due to the presence of free radicals and/or the elevated Gal-1-P.

Effect of corticosteroids on elevated intracellular sodium, plasma lipid peroxide levels and reduced Na(+), K(+)-ATPase activity in patients of bronchial asthma.

In view of several reports that there is a lack of balance in free radicals in case of bronchial asthma (1) the effect of free radicals on cell membrane was studied by estimating the membrane bound protein Na(+), K(+)-ATPase activity and the intracellular sodium level in patients of bronchial asthma before and after a short course (one week) of oral corticosteroid (prednisolone 0.75-1mg/kg body weight) therapy. Results showed that there is a definite statistically significant rise in free radical level and intracellular sodium level and a significant lowering of Na(+), K(+)-ATPase activity in case of untreated bronchial asthma. After short course of therapy with oral corticosteroids, the free radical level and intracellular sodium level decreased significantly, together with a significant rise of the Na(+), K(+)-ATPase activity. Also, a significant negative correlation (r=-0.74) between the lipid peroxide level and the Na(+),-K(+)-ATPase activity was found in these cases.

Erythrocyte Na +, K +-ATPase activity in patients with congestive heart failure

In order to determine if the Na +, K +-ATPase activity in erythrocyte membranes is altered in congestive heart failure, and to examine its clinical significance with respect to other clinical variables, erythrocyte Na +, K +-ATPase activity was measured in 51 patients with left ventricular ejection fractions <40% (coronary artery disease, n=26; dilated cardiomyopathy, n=25) and 24 control patients. Na +, K +-ATPase activity was lower in both coronary artery disease and dilated cardiomyopathy groups than control group even in the absence of digitalis use. There was a significant inverse correlation between Na +, K +-ATPase activity and plasma norepinephrine. The presence of non-sustained ventricular tachycardia was associated with a lower Na +, K +-ATPase activity in both groups with congestive heart failure without digitalis use than those without ventricular tachycardia. Plasma norepinephrine was higher in patients with non-sustained ventricular tachycardia than those without in the coronary artery disease group, but not in the dilated cardiomyopathy group. Na +, K +-ATPase activity may be helpful in predicting electrophysiologic instability in patients with heart failure.

Erythrocyte membrane ATPase activities in patients with chronic active hepatitis B and C virus infections

The aim of the present study was to obtain erythrocyte membrane fractions from patients with chronic active hepatitis caused by hepatitis B virus (HBV) and hepatitis C virus (HCV) infections. Na +,K + ATPase activities were significantly lower ( P<0.005) in HBV related chronic active hepatitis ( n=20, 0.134±0.073 μmol P/mg protein per h) and in HCV hepatitis ( n=11, 0.144±0.049 μmol P/mg protein per h) when compared to control group ( n=10, 0.219±0.055 μmol P/mg protein per h). Both types of chronic active hepatitis B and C have markedly altered erythrocyte membrane Na +,K + ATPase activities that can be indicative of hepatic cell damage in humans. Although HBV and HCV infections are based on diverse mechanisms of action on their effect in liver injury, they cause similar effects on membrane ATPase activities.

Effect of yoga training on plasma lipid profile, R.B.C. membrane lipid peroxidation and Na+K+ ATPase activity in patients of essential hypertension

We conducted a controlled study on effect of selected yoga practive in the control and management of 50 cases of essential hypertension and equal number of healthy (nonhypertensive) controls. Free radical cellular damage is considered to be the underlying common biological factor in essential hypertension. We, therefore, investigated lipid profile lipid peroxidation and Na+K+ ATPase activities of plasma membrane of subjects with essential hypertension. It was found that hypertensive subjects had an elevated lipid peroxidation and decreased Na+K+ ATPase activity in plasma membrane as compared to normotensive healthy controls, the specific yoga training protocol which was administered not only helped to decrease blood pressure but also retard the progression of ceellular damage due to free radicals.

Alterations in intracellular cations and cell membrane ATPase activity in patients with malignant hypertension

To determine whether cellular cation concentrations and cell membrane ATPase activity are altered in patients with malignant hypertension. Sixteen black patients with malignant hypertension were studied and compared with age- and sex-matched essential hypertensive and normotensive subjects. Calcium, magnesium, sodium and potassium concentrations and cell membrane Na,K-ATPase, Ca-ATPase and Mg-ATPase activities were determined in platelets and erythrocytes. Intracellular concentrations of total magnesium and calcium were measured by atomic absorption spectrophotometry, and those of sodium and potassium by flame photometry. Cell membrane ATPase activity was measured by a colorimetric method. The intracellular calcium level was significantly elevated and intracellular magnesium and potassium levels and cell membrane ATPase activity significantly decreased in the hypertensive group. These changes were more marked in patients with malignant hypertension than in patients with benign essential hypertension. In the malignant hypertensive group, mean arterial pressure was negatively correlated with intracellular magnesium and positively correlated with intracellular calcium and sodium levels. Cellular cation changes in malignant hypertension may be related to altered transmembrane transport mechanisms and activation of the renin-angiotensin system. These alterations may be more pronounced in the malignant than in the benign phase of hypertension.

Reduced Na+, K+-ATPase Activity in Patients with Pseudohypoaldosteronism

Pseudohypoaldosteronism is a hereditary salt-wasting syndrome usually seen in infancy with weight loss, dehydration, and failure to thrive. The pathophysiologic origin of pseudohypoaldosteronism is unknown. The defect could be related to the unresponsiveness of target organs to mineralocorticoids resulting in hyponatremia, hyperkalemia, and markedly elevated plasma aldosterone and renin levels. Red blood cell Na+, K(+)-ATPase activity was measured in a pair of twins with pseudohypoaldosteronism, in an unrelated child with hypoaldosteronism, and in an age-matched group of 50 healthy infants and young children. The enzyme was assayed by a method that couples ATP hydrolysis with NADH oxidation. Plasma renin and aldosterone levels were measured by RIA. Red blood cell Na+, K(+)-ATPase activity in the twins with pseudohypoaldosteronism was very low at the time of diagnosis (3 wk). In both twins a time-related gradual increase in enzyme activity was observed during the 1st mo of life, reaching control values between 6 and 8 mo of age. This increase was associated with both a reduction in salt requirement and clinical improvement. Plasma renin activity and aldosterone levels were very high at the time of diagnosis. Plasma renin activity reverted gradually to normal values, whereas aldosterone levels remained high throughout the follow-up period. The child with hypoaldosteronism had normal Na+, K(+)-ATPase activity at diagnosis and during follow-up.

Erythrocyte calcium-stimulated, magnesium-activated adenosine 5??-triphosphatase activity in essential hypertension

The aim of this study was to investigate the basis of reduced erythrocyte calcium-stimulated, magnesium-activated adenosine 5' triphosphatase (Ca2+, Mg(2+)-ATPase) activity in essential hypertension. Experiments were performed to establish whether the reduced erythrocyte Ca2+, Mg(2+)-ATPase activity in patients with essential hypertension, when compared with age- and sex-matched normotensive control subjects, was due to changes in enzyme properties or to an altered membrane environment. Erythrocyte membrane Ca2+, Mg(2+)-ATPase activity was determined by measuring ATP-dependent 45Ca2+ uptake in inside-out vesicles and calcium-dependent gamma-32P ATP hydrolysis in ghost membranes, prepared from the same sample of blood. Calcium-dependent gamma-32P ATP hydrolysis activity was also measured in detergent extracts of erythrocyte membranes. In the absence and presence of calmodulin, both ATP-dependent Ca2+ uptake and calcium-dependent ATP hydrolysis activities of erythrocyte membranes prepared from patients with essential hypertension were significantly reduced when compared with normotensive subjects. No difference in calmodulin affinity was observed between hypertensive and normotensive subjects, although the calcium dependence of calmodulin-independent Ca2+ uptake activity in inside-out vesicles was altered. No significant difference in calcium-dependent ATP hydrolysis activity was observed between hypertensive and normotensive preparations after detergent solubilization of erythrocyte membrane proteins. These results suggest that the number of Ca2+, Mg(2+)-ATPase units is similar in erythrocytes of hypertensive and normotensive subjects and that the reduced activity in the intact erythrocyte membrane of hypertensive patients is due to an altered membrane environment.

The Effect of Glucose Load on Insulin and Platelet NA+, K+ ATPase Activity in Patients with Thyrotoxic Periodic Paralysis (TPP)

The Effect of Glucose Load on Insulin and Platelet NA+, K+ ATPase Activity in Patients with Thyrotoxic Periodic Paralysis (TPP)

Reduced Langerhans' cell Ia antigen and ATPase activity in patients with the acquired immunodeficiency syndrome.

We investigated the possible role of a defect in antigen-presenting cells in the acquired immunodeficiency syndrome (AIDS), by enumeration of Langerhans' cells, the epidermal antigen-presenting cells. These cells were stained for the characteristic markers, surface Ia antigen and surface ATPase activity. A significant reduction was observed in the number of stained cells per square millimeter of body-surface area in 24 patients with AIDS and either opportunistic infections (Ia, 258 +/- 34, and ATPase, 274 +/- 46) or Kaposi's sarcoma (Ia, 378 +/- 100, and ATPase, 530 +/- 26), as compared with 38 appropriate controls (Ia, 721 +/- 13, and ATPase, 693 +/- 12). Examination of six patients with an "AIDS-related complex" revealed significantly reduced numbers of Langerhans' cells per square millimeter; this reduction was more pronounced in staining for Ia antigen (306 +/- 69) than in staining for ATPase activity (517 +/- 101). Given the known role of Ia expression in antigen presentation, we suggest that functional alterations in Langerhans' cells, and perhaps also in antigen-presenting cells in tissues other than skin, may be involved in the pathogenesis of AIDS.

Erythrocyte Na+, K+-ATPase and serum digoxin concentrations.

Digoxin therapy has been made more rational by the measurement of serum digoxin concentrations. However, difficulties remain because of the overlap between "therapeutic" and "toxic" serum concentrations and the lack of an obvious therapeutic endpoint in many patients. An assay which measures the degree of interaction between digoxin and its putative receptor, the membrane Na+, K+-ATPase, might be capable of resolving some of these difficulties. Therefore, as a first approach in this direction we evaluated the relationship between serum digoxin concentration and the degree of inhibition of RBC ghost Na+, K+-ATPase activity in patients receiving digoxin therapy. Utilizing an improved micro-assay technique, Na+, K+-ATPase activity was determined in aliquots of RBC ghosts before and after removal of bound digoxin. In 27 patients a significant relationship was present between serum digoxin concentration and the degree of RBC ghost Na+, K+-ATPase inhibition. However, at any serum digoxin concentration, there was a variation in the magnitude of enzyme inhibition from patient to patient. This study confirms the feasibility of determining the degree of in vivo RBC Na+, K+-ATPase inhibition in man and demonstrates, for the first time, a highly significant but somewhat variable relationship between serum digoxin concentrations and the magnitude of RBC digoxin receptor inactivation. This quantitative, functional, individualized assay of digoxin effects may prove to be of clinical value in the future.

Lymphocyte ATPase activity in patients with carcinoma of the larynx. A follow-up study on 45 patients.

Mitochondria-related Mg ATPase activity was assayed in lymphocytes isolated from the blood in 45 patients with epidermoid carcinomas of the larynx. Increased activity was found in 11 patients and normal or subnormal activity in the remaining cases. No correlation could be demonstrated between the magnitude or the spreading of the malignancy as recorded by the TNM classification and the ATPase activity. In 36 patients determinations were carried out repeatedly during a period from 6 to 20 months following therapy and after 3 years a final follow-up on all patients was done. All patients received high-voltage radiotherapy and in 7 patients additional partial or total laryngectomia was carried out, one patient had bilateral neck dissection. After radiotherapy the ATPase activity decreased significantly in 17 patients while it either remained normal or increased temporarily in the rest. No correlation was found between the course of the disease and the initial ATPase activity or the pattern of variation in ATPase activity following therapy. Contrary to what resulted from a preliminary study, it is concluded that determination of lymphocyte ATPase activity is of no diagnostic value in patients with laryngeal carcinoma, nor does it offer any prognostic help in determining which patients may relapse or develop metastatic disease.

Toxic effect of lead on erythrocyte membranes

Lead has been reported to poison many enzyme systems including the Na+K dependent ATPase essential to maintaining normal membrane potentials. The present study was designed to measure the toxic effects of lead on membrane trnaspor in human erythrocytes resulting from possible changes in ATPase activity. Na flux and membrane Na+K dependent. ATPase were measured in erythrocytes of patients with lead poisoning and in normal erythrocytes exposed in vitro to lead in concentrations of 50–200 micrograms/100 ml. We have not been able to confirm the presence of decreased. ATPase activity in patients with mild lead poisoning (i.e. no encephalopathy and blood concentrations of lead between 60 and 90 micrograms/100 ml.). However, we have demonstrated a markedly increased passive Na leak in both erythrocyte ghosts and intact cells. Active outward Na transport was also increased perhaps as a compensatory mechanism. In vitro exposure of intact red cells to lead has produced similar increases in membrane permeability to Na. In addition, when lead is incorporated in vitro into erythrocyte ghosts inhibition of active transport can be demonstrated. The mechanisms producing the two different effects of lead on membrane transport are separable and may be dose dependent. Thus lead affects the membrane in addition to any possible enzyme injury.

Myofibrillar adenosine triphosphatase activity of human heart tissue in congestive failure: effects of ouabain and calcium.

Ouabain had no effect on myofibrillar adenosine triphosphatase (ATPase) activity in normal, hypertrophic, and failing hearts with concentrations of calcium chloride varying from 0 to 5.0 mM. The quantitative effects of CaCl 2 on myofibrillar ATPase were the same in all groups studied. At necropsy it was found that myofibrillar ATPase activity of heart tissue from patients with clinical and pathologic diagnoses of failure from left ventricular volume and pressure overload was significantly lower than that of normal controls. The ATPase activity in patients with failure due to right ventricular volume and pressure overload was not significantly lower than that in normal controls. There was no difference in myofibrillar ATPase activity between normal left and normal right and between failing left and failing right ventricles. The difference demonstrated at necropsy between normal and failing hearts was not a function of age or of hypertrophy per se. Myofibrillar ATPase activity of hypertrophic nonfailing surgical pulmonary infundibular tissue was the same as that of normal postmortem ventricles. The ATPase activity of failing surgical papillary muscle in a small number of experiments was in the range of that found in failing postmortem ventricles.