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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of sodium pentosan polysulphate (SPP) was investigated in calcium oxalate stone forming rats with respect to the urinary excretion of certain risk factors and enzymes. Calcium oxalate stones were induced by feeding 3% w/w sodium glycollate to the rats. Urinary calcium, oxalate, phosphorus and uric acid levels were increased in stone formers. In contrast magnesium excretion was low in this group. SPP treatment lowered oxalate and calcium levels in both controls and experimental animals. Magnesium levels were increased moderately. Increased excretion of urinary enzymes--LDH, alkaline phosphatase, gamma-GT and beta glucuronidase--in calculogenic rats indicates membranuria and damage to proximal tubules during stone formation. Decreased pyrophosphatase activity was observed in glycollate fed rats. SPP treatment decreased the excretion of the above enzymes in the treated groups. Stone formers exhibited decreased LAP and fibrinolytic (urokinase) activities. SPP being associated with fibrinolytic properties, increased the activities of the above two enzymes to that of control levels in calculogenic rats.
Biochem Mol Biol Int 1993 Feb
PMID:Alterations in some risk factors and urinary enzymes in urolithiatic rats treated with sodium pentosan polysulphate. 768 93

Calcium and oxalate uptake by renal brush border membrane vesicles (BBMV) was examined in magnesium-deficient and pair-fed control rats. Uptake studies were carried out by rapid filtration technique and rate of influx of calcium and oxalate as a function of extravesicular concentration (0.1 nM--1.0 mM) examined. Calcium uptake by renal BBMV exhibited saturable kinetics while oxalate uptake followed a biphasic transport mechanism showing saturable kinetics at low oxalate concentrations and passive diffusion at higher concentrations. In magnesium deficiency the kinetics of calcium and oxalate uptake by renal BBMV remained unaltered but the rate of uptake was significantly enhanced at all the extravesicular concentrations studied. Double reciprocal plot for calcium uptake showed no change in Vmax but a decrease in Km (2.08 mM) in magnesium--deficient rats as compared to pair-fed controls (Km = 5.00 mM). Similar plot for oxalate uptake showed an increase in Vmax (7.69 nmoles/8 min/mg protein) in magnesium deficient group as compared to pair-fed controls (5.55 nmoles/8 min/mg protein), while Km remained unchanged. The results of the present study indicate high risk of calcium oxalate stone formation in magnesium--deficient rats due to hyperabsorption and retention of calcium and oxalate by the renal tubular brush border membrane.
Biochem Mol Biol Int 1994 Nov
PMID:Calcium and oxalate uptake by the renal brush border membrane vesicles in magnesium-deficient rats. 770 98

Soluble organic matrix was extracted with 0.1 M EDTA from calcium oxalate monohydrate urinary stone (CaOx), purified by SDS-polyacrylamide gel electrophoresis and transferred to polyvinylidene difluoride membranes for the NH2-terminal amino acid sequence analysis. A protein at 30 kDa showed complete homology with calprotectin (20 amino acids in the NH2-terminal), so we termed this a calprotectin-like protein. Calprotectin which was extracted from human granulocytes had inhibitory activity in calcium oxalate monohydrate crystal growth in vitro. This study suggested that, calprotectin-like protein detected in CaOx is thought to be a potent inhibitor of crystal growth and may therefore be important in the etiology of CaOx formation.
Biochem Mol Biol Int 1994 Sep
PMID:Calprotectin-like protein is related to soluble organic matrix in calcium oxalate urinary stone. 784 42

The sarcoplasmic reticulum (SR) membranes isolated from rabbit heart were preincubated at pH 6.8 or 7.8 and their Ca2+ pump properties were compared at pH 6.8. The ATP-dependent azide insensitive oxalate-stimulated Ca2+ uptake was reduced more rapidly from the membranes preincubated at 37 degrees C at pH 7.8 than from those preincubated at pH 6.8. The Ca(2+)-Mg(2+)-ATPase, and the Ca(2+)-dependent formation of 110 kDa acylphosphate were also inhibited by the preincubation at the higher pH. Including 1 mM DTT in the preincubation medium reduced the inactivation. The preincubation at 37 degrees C in the presence or absence of DTT caused membranes to become more leaky as the loss of Ca2+ uptake was more rapid than that of ATPase or the acylphosphate formation. The loss of these activities was not accompanied by a breakdown of the protein as monitored in Western blots. It is hypothesized that the SR Ca2+ pump inactivation involves a key-SH group and that the lower pH provides a compensatory protective mechanism for the SR during acidosis.
Mol Cell Biochem 1993 Sep 08
PMID:Effect of pH on stability of sarcoplasmic reticulum calcium pump in rabbit heart. 810 93

The present study was carried out to investigate the relation between erythrocyte oxalate flux rate and the pathogenesis of calcium oxalate renal stone disease having hyperoxaluria as the main risk factor. Male albino rats were made hyperoxaluric by feeding them diets viz. vitamin B6 deficient, vitamin B6 deficient + 51.7% galactose or fructose (serving as a sole source of carbohydrate), along with their respective pair-fed controls for 4 weeks. After 28 days of feeding, oxalate excretion was in the order of vitamin B6 deficient + galactose > galactose control > vitamin B6 deficient + fructose > vitamin B6 deficient > fructose control/vitamin B6 control. Whereas, transmembrane oxalate flux rate was in the order of vitamin B6 deficient > vitamin B6 deficient + galactose > vitamin B6 deficient + fructose > vitamin B6 control > galactose control > fructose control. No significant correlation (r = 0.304) was found between the urinary oxalate excretion and erythrocyte oxalate flux rates of various groups of rats. The study indicates that increase in oxalate excretion does not concomitantly increase the transmembrane oxalate flux in red blood cells.
Biochem Mol Biol Int 1993 Sep
PMID:A comparative study of erythrocyte oxalate flux rate and urinary oxalate excretion in hyperoxaluric rats. 826 Sep 49

The effect of nicotinamide-adenine dinucleotides (NAD+ and NADP+) on Ca2+ transport in rat liver nuclei was investigated. Ca2+ uptake and release were determined with a Ca2+ electrode. Ca2+ uptake was dependent on adenosine triphosphate (ATP; 2 mM). The presence of NAD+ (2 mM) or NADP+ (1 and 2 mM) caused a significant inhibition of Ca2+ uptake following addition of 2 mM ATP. Ca2+, which accumulated in the nuclei during 6 min after ATP addition, was significantly released by the addition of NAD+ (0.5-2 mM) or NADP+ (0.1-2 mM). However, the effect of NADH (2 mM) or NADPH (2 mM) on Ca2+ uptake and release clearly weakened in comparison with the effects of NAD+ and NADP+. Meanwhile, ryanodine (10 microM), thapsigargin (10 microM) or oxalate (0.5 mM) had no effect on Ca2+ uptake and release in rat liver nuclei. These reagents did not significantly alter the effects of 2 mM NAD+ on Ca2+ uptake and release. Thus, NAD+ and NADP+ had a potent effect on Ca2+ transport in rat liver nuclei. The present findings suggest that the liver cytosolic NAD+ (NADP+) is a factor in the regulation of the nuclear Ca2+ concentration.
Mol Cell Biochem 1993 Apr 21
PMID:Effect of nicotinamide-adenine dinucleotides on Ca2+ transport system in rat liver nuclei: stimulation of Ca2+ release by NAD+. 831 29

To evaluate the role of parathyroids in calculus disease, the parathyroid hormone levels were determined in 22 control subjects and 42 stone (14 with bladder stone and 28 with kidney stone) patients. Serum calcium, inorganic phosphate, alkaline phosphatase and parathyroid hormone and urinary excretion of calcium and inorganic phosphate were determined. It was found that normocalcemic and normocalciuric stone patients had slightly higher levels of parathyroid hormone (irrespective of the site of the stone) and the difference was not statistically significant as compared with control subjects although some of the patients with calculus disease were hyperparathyroid. Serum alkaline phosphatase was increased while there was an increase in urinary calcium excretion in kidney stone patients and oxalate in all patients as compared with control subjects. The increase in inorganic phosphate was, however, not different from the control subjects. The subclinical hyperparathyroidism and stone formation in these patients are not correlated.
Mol Cell Biochem 1993 Apr 07
PMID:Parathyroid hormone in urinary stone patients. 851 Jun 69

The aim of this study was to examine the relationship between sarcolemmal Na(+)-Ca2+ exchangers and sarcoplasmic reticulum (SR) Ca(2+) -ATPase (SERCA2) expression and the developmental differences in cardiac Ca2+ handling. Postnatal steady-state mRNA and protein levels were analysed in rat ventricular myocardium by Northern and immunoblot analysis, respectively. This was compared to Na+ gradient-induced and SR oxalate-supported Ca2 transport in isolated membranes. Na(+)-Ca2+ exchanger mRNA declined by 75% between day 1 and 30, whereas SR Ca2+ ATPase mRNA levels increased by 97% during this period. The Na(+)-Ca2+ exchanger mRNA/Ca(2+)-ATPase mRNA ratio was found to be inversely related to post-natal age. The changes in mRNA levels were associated with corresponding developmental differences in the Ca2+ transport activities of the respective membrane proteins. In crude membranes, the Na(+)-dependent Ca2+ transport activity (at 75 microM Ca2+) declined gradually (P < 0.01; mean +/- S.E.) from 17.7 +/- 2.4 nmoles Ca2+/g wet tissue/2s at day 1-3 (n = 5) to a value of 4.2 +/- 1.1 at day 40 (n =4). Conversely, SR Ca2+ uptake increased (P < 0.01) 2.6-fold during this period. The inversely related changes in the post-natal expression and function of the Na(+)-Ca2+ exchanger and SR Ca(2+)-ATPase suggest a coordinated control at the pretranslational level of the cellular Ca2+ transport processes mediated by the two membrane proteins.
J Mol Cell Cardiol 1995 Aug
PMID:Reciprocal changes in the postnatal expression of the sarcolemmal Na+-Ca(2+)-exchanger and SERCA2 in rat heart. 852 31

The effect of 15 min of global, normothermic ischemia on 3H-ryanodine binding and the oxalate-supported Ca2+ uptake of cardiac sarcoplasmic reticulum (SR) was investigated in parallel using ventricular homogenates of isolated perfused rat hearts. Ischemia increased the Ca2+ efflux under the uptake assay conditions, as demonstrated by the greater stimulation of Ca2+ uptake by high concentrations of ryanodine (+RY) to close the SR Ca2+ channel. This effect was partially reversed by reperfusion. Ischemia depressed Ca2+ uptake rate -RY at free [Ca2+] of 0.4 microM and above, while the depression + RY was significant only above 10 microM Ca2+. We tested the hypothesis that inhibition of the Ca-ATPase alone, by adding thapsigargin or cyclopiazonic acid, could reproduce the effects of ischemia on the homogenate Ca2+ uptake rate. Thapsigargin or cyclopiazonic acid proportionally depressed Ca2+ uptake rate +RY and -RY and produced distinctly different effects of ischemia. Ischemia did not change the Bmax or Kd for equilibrium 3H-ryanodine binding, or the Hill coefficient or KCa for the [Ca2+]-dependence of equilibrium 3H-ryanodine binding. The rate of ryanodine binding, measured under the uptake conditions, was increased by ischemia and further increased by reperfusion. The effect of ischemia on the rate and extent of equilibrium binding to the high-affinity ryanodine binding site were unrelated to the highly reproducible effects on SR Ca2+ uptake rates measured in the homogenate.
J Mol Cell Cardiol 1995 Sep
PMID:Effect of ischemia and ischemia--reperfusion on ryanodine binding and Ca2+ uptake of cardiac sarcoplasmic reticulum. 852 56

The SS-enantiomer 3-(2-ethylphenoxy)-1-[(1S)-1,2,3,4-tetrahy dronaphth-1-ylaminol]-(2S)-2-propanol oxalate (SR 59230A) is proposed to be the first beta 3-adrenergic receptor antagonist. The present work shows that SR 59230A, unlike its inactive RR-enantiomer (SR 59483), antagonized a typical beta 3-adrenergic response in vitro, i.e., SR 58611A, the ethyl-[(7s)-7-[[(2R)-2-(3- chlorophenyl)-2-hydroxethyl]amino]-5,6,7,8-tetrahydronaphth- 2- yl]oxyacetate hydrochloride- or (-)-4-(3-t-butylamino-2-hydroxypropoxy)benzimidazol-2-one (CGP 12177)-stimulated synthesis of cAMP in rat brown adipose tissue membranes, with pKB values of 8.87 +/- 0.12 and 8.20 +/- 0.15. In addition, SR 59230A had no antagonistic effect on forskolin-induced cAMP accumulation in rat interscapular brown adipose tissue. SR 59230A, in contrast to the selective beta 1- and beta 2-adrenoceptor antagonists (+/-)[2-(3-carbamoyl-4-hydroxyphenoxy)-ethylamino]- 3-[4(1-methyl-4-trifluoromethyl-2-imidazolyl)-phenoxy]-2 propanol and erythro-(+/-)-1-(7-methylindan-4-yloxy)-3-isopropylaminob utan- 2-ol-hydrochloride did not counteract the cAMP production induced by (-)-isoprenaline or norepinephrine (NE) in rat brain areas rich in beta 1- or beta 2-adrenoceptors, such as frontal cortex and cerebellum. Moreover, in proliferating brown fat cells, in which the beta 1-adrenoceptor is the only beta-adrenergic subtype coupled to cAMP production, SR 59230A did not modify the production of cAMP induced by NE, whereas CGP 12177 did. In confluent brown fat cells, in which the beta 3-adrenoceptor is the functional beta-adrenergic subtype coupled to adenylyl cyclase, SR 59230A antagonized the NE-induced cAMP accumulation and glycerol release without affecting their basal values, whereas CGP 12177, which per se stimulated cAMP accumulation and glycerol release, did not change the NE-induced increase of either parameter. Finally, SR 59230A concentration-dependently counteracted the NE-stimulated synthesis of uncoupling protein gene in confluent brown fat cells, which is considered mainly a result of selective stimulation of beta 3-adrenoceptors. These results provide evidence that the new selective beta 3-adrenoceptor antagonist can contribute considerably to functional characterization of the beta 3-adrenoceptors.
Mol Pharmacol 1996 Jan
PMID:Functional studies of the first selective beta 3-adrenergic receptor antagonist SR 59230A in rat brown adipocytes. 856 14


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