ATPase Of Red Cells Research Articles

Comparative study of Coptidis Rhizoma and Aconiti Kusnezoffii Radix on cell differentiation in lewis lung cancer

Coptidis Rhizoma and Aconiti Kusnezoffii Radix represent hot Chinese medicine and cold Chinese medicine respectively. The purpose of this study is to observe the differentiation effect of Coptidis Rhizoma and Aconiti Kusnezoffii Radix on lewis lung cancer and compare effect of hot Chinese medicine and cold Chinese medicine on tumor progression. In this study, the rat serum containing Coptidis Rhizoma or Aconiti Kusnezoffii Radix was prepared to treat lewis lung cancer cells in vitro, and effects of the serum containing Coptidis Rhizoma or Aconiti Kusnezoffii Radix on cell differentiation, proliferation, adhesion, succinic dehydrogenase (SDH) activity and gap-junction intercellular communication (GJIC) were investigated. In vivo, the subcutaneous implant model and pulmonary metastasis model of lewis lung cancer were established. Tumor bearing mice were taken water decoction of coptis chinensis or aconite by intragastric administration bid for four weeks, and the influences of coptis chinensis and aconite on tumor progression were evaluated by body temperature, blood oxygen saturation, red cell ATPase, blood rheology, intratumor hypoxia, capillary permeability and GJIC. The results showed that the serum containing aconite could induce cell differentiation, inhibit cell proliferation and migration, promote SDH activity and GJIC in lewis lung cancer cells. The serum containing Coptidis Rhizoma increased cell adhesion and decreased SDH activity and GJIC without cell differentiation although it also suppressed cell proliferation. Aconiti Kusnezoffii Radix water decoction could keep body temperature, blood oxygen saturation, red cell ATPase and blood rheology, and improve intratumor hypoxia, capillary permeability and GJIC in tumor bearing mice, which led to slower tumor growth and less metastasis. Coptidis Rhizoma water decoction decreased body temperature, blood oxygen saturation, red cell ATPase, blood rheology and GJIC, and promoted intratumor hypoxia and capillary permeability, which resulted to more tumor metastasis although it also prevented tumor growth. These results suggested that the hot Chinese medicine could induce tumor cell differentiation and prevent tumor poison invagination, which is better for tumor treatment than cold Chinese medicine.

Studies of the etiology of obesity in Pima Indians

Studies have been conducted on various metabolic characteristics of lean and obese Pima Indians, including studies of fat-cell morphology, glucose transport, and lipolysis; lipoprotein lipase activities; sodium-potassium ATPase in red cells, adipocytes, and fibroblasts; lipids and lipoprotein metabolism; fatty acid metabolism; and sterol balance. Insulin concentrations, insulin binding, insulin action on glucose disposal, fatty acid metabolism, and islet function were compared in lean and obese individuals, and the relationship between insulin resistance and muscle morphology was explored. To explore potential abnormalities in energy balance, calorie intake and gastric emptying were compared in lean and obese Pimas and measurements of energy expenditure were performed. The data suggest that there are multiple metabolic differences that accompany obesity in Native Americans. A lower metabolic rate was a determinant of future weight gain, and abnormalities in use of free fatty acids and cell insulin action were suggested, which emphasize the need for further studies in these areas.

The effect of in vivo glucose administration on human erythrocyte Ca2+-ATPase activity and on enzyme responsiveness in vitro to thyroid hormone and calmodulin.

To characterize endogenous control mechanisms for human erythrocyte membrane Ca2+-ATPase ("calcium pump") activity, we studied the effect of changes in blood glucose concentration in vivo within the physiologic range on Ca2+-ATPase activity in red cells. Red cells obtained in the course of induced hyperglycemia were also studied to determine susceptibility of membrane Ca2+-ATPase to stimulation in vitro by thyroid hormone and calmodulin, both of which have been shown previously to enhance Ca2+-ATPase activity. Oral glucose administration (75 g) to eight healthy, adult subjects induced predictable increases in concentrations of blood glucose and immunoreactive insulin. Basal levels of activity of Ca2+-ATPase in red cells obtained after glucose ingestion fell 55% (P less than 0.025) by 30 min after glucose with recovery of enzyme activity to levels not significantly different from basal by 60 min. Activity of red cell Ca2+-ATPase at time zero was significantly stimulated in vitro by thyroxine (T4, 10(-10) M), triiodo-L-thyronine (T3, 10(-10) M), and calmodulin (100 ng/mg membrane protein). In vivo glucose administration led to depression of red cell enzyme responsiveness in vitro to T4 and T3; recovery from this effect did not occur by 120 min after oral administration of glucose. Calmodulin responsiveness of the enzyme in vitro was less significantly reduced in red cells obtained after glucose ingestion. Intravenous (i.v.) glucose administration (20 g) to five subjects also led to decreased basal enzyme activity (61% of fasting level at 20 min). A significant decrease in response of enzyme to T4 was achieved by 8 min after glucose administration (P less than 0.02), with recovery by 60 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Red cell ATP-ASE activities in hypertensive patients on long term diuretic therapy

Red cell ATP-ASE activities in hypertensive patients on long term diuretic therapy

Na-K-dependent ATPase in red cells and thyroid status.

The Relationship between ouabain-sensitive ATPase (Na-K ATPase) activity in erythrocytes and the thyroid status was studied in 36 patients with Graves' disease and 58 patients receiving L-thyroxine (T4) replacement therapy. Forty normal children served as control. Total ATPase activity in 4 untreated hypothyroid patients was significantly reduced (11.0 +/- 4.6 vs 17.3 +/- 4.1 micrograms-P/h/mg-protein, P less than 0.01), and Na-K ATPase was undetectable, both of which were normalized after 4 weeks of L-T4 therapy. Na-K ATPase in hyperthyroid patients was also decreased (0.9 +/- 0.8 vs. 4.0 +/- 2.7, P less than 0.01), but was gradually normalized after 3 months of euthyroid state. Clinically euthyroid children treated with L-T4 were divided into 2 groups with regard to Na-K ATPase activity, normal and low. Analysis of the possible factors producing this difference revealed that, in primary hypothyroidism, the factor appeared to be the endogenous T4 level, while in patients with dwarfism, the secretory capacity of TSH or TSH-releasing hormone (TRH) was contributory. Thus Na-K ATPase activity in red cells remains within the normal range after L-T4 replacement in the presence of a severe degree of primary hypothyroidism or in association with secondary or tertiary hypothyroidism. Other factors such as the L-T4 dose, duration of the therapy, serum T4 and T3 concentrations, were not significantly different in the two groups. These results indicate that (1) Na-K ATPase in red cells is decreased in hyper- or hypothyroid state, (2) restoration of normal activity requires 1-3 months of euthyroid period, and (3) it is a sensitive index of peripheral thyroid status over the preceding few months.

(Ca ++ + Mg ++ )‐ATPase of red cells in Duchenne and myotonic dystrophy

Red cell (Ca⁺⁺ + Mg⁺⁺)-ATPase was investigated in Duchenne and myotonic dystrophy patients. Saponin-lysed red cells of patients with Duchenne dystrophy displayed slightly higher (Ca⁺⁺ + Mg⁺⁺)-ATPase activity (66.2 ± 2.6 ±moles Pi [inorganic phosphorus] per 2 hours per milliliter cells) than age-matched male controls (54.3 ± 2.4 ±moles Pi per 2 hours per milliliter cells). The activity of the enzyme in myotonic dystrophy patients was somewhat lower (59.6 ± 1.3 μnoles Pi per 2 hours per milliliter cells) than in controls (66.7 ± 1.6 ±moles Pi per 2 hours per milliliter cells). In all cell types, a cytoplasmic activator protein is present, which stimulated the (Ca⁺⁺ + Mg⁺⁺)-ATPase of hypotonically isolated membranes. In age-matched Duchenne controls, the membrane enzyme was maximally stimulated by the activator, increasing from 14.4 ± 0.5 ±moles Pi per 2 hours per milliliter cells to 28.5 ± 1.4 ±moles Pi per 2 hours per milliliter cells. Duchenne (Ca⁺⁺ + Mg⁺⁺)-ATPase was enhanced from 15.8 ± 0.7 ±moles Pi per 2 hours per milliliter cells in the membrane to 33.3 ± 1.8 ±moles Pi per 2 hours per milliliter cells by the activator. Similarly, myotonic (Ca⁺⁺ + Mg⁺⁺)-ATPase activity was augmented from 13.7 ± 0.5 ±moles Pi per 2 hours per milliliter cells to 29.4 ± 1.5 ±moles Pi per 2 hours per milliliter cells by the activator, whereas enzymes from age-matched controls displayed a stimulation from 15.0 ± 0.6 ±moles Pi per 2 hours per milliliter cells to 36.2 ± 1.7 ±moles Pi per 2 hours per milliliter cells in the presence of their own activator. The extent of the enzyme stimulation by the activator was independent of the source of its origin in all cases, suggesting that the differences observed in the (Ca⁺⁺ + Mg⁺⁺)-ATPase from patients and controls were more likely related to differences in membrane structure than to alteration in the activator protein.