Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty male Wistar rats, weighing 150 g, were placed in metabolic cages on a 30% sucrose diet for 7 days, before allocation to two groups: a control group (n = 5) and a lactose group (n = 15). They received respectively a 30% sucrose diet or a 30% lactose diet for 8 weeks, each containing 0.67% calcium and 0.38% phosphorus. After 4 (T1) and 8 (T2) weeks, the serum calcium (Ca) and citrate levels were significantly (P < 0.01) higher in rats fed the lactose diet. Serum alkaline phosphatase activity was increased in the lactose group (P < 0.01) at T1 and T2. The lactose-rich diet induced an increase in urinary Ca excretion at T1 and T2; citrate excretion was only enhanced at T2 (P < 0.001). No difference between the two groups was observed in urinary oxalate (Ox) excretion or creatinine clearance. Crystalluria analysis revealed a marked number (>300/mm3 at T1 and T2) of calcium oxalate dihydrate crystals (COD) in rats fed the lactose-rich diet, whereas no COD crystals were observed in sucrose-fed control rats at any time point. The formation of COD crystals in lactose-fed rats was related to an increase in calcium oxalate (CaOx) product (pCaOx), which was respectively 12.6 vs 3.9 at T1 and 10.5 vs 1.8 at T2, and an increase in CaOx ratio (Ca/Ox), which was 99.1 vs 7.5 and 67.5 vs 18.5 at T1 and T2, respectively. The high pCaOx and Ca/Ox ratios in the lactose group were due to hypercalciuria, in agreement with the number and the type of crystals. The present experimental model confirms that the ingestion of a 30% lactose diet increases urinary Ca excretion without changing urinary Ox excretion and shows for the first time that it induces a stable and marked crystalluria composed of COD. Such a non-nephrotoxic and stable model is of interest for the study of CaOx crystal formation secondary to hypercalciuria, and thus afterwards eventually for CaOx nephrolithiasis.
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PMID:A stable animal model of diet-induced calcium oxalate crystalluria. 953 98

Using ethylene glycol (EG) and vitamin D3 as crystal-inducing diet (CID) in rats, we investigated the effect of the dosage of EG on the generation of chronic calcium oxalate (CaOx) nephrolithiasis. We collected weekly 24 hour urines and measured herein the amount of oxalate, calcium, glycosaminoglycans (GAG's), creatinine, protein, alkaline phosphatase (AP), gamma-glutamyl transpeptidase (gamma-GT), and N-acetyl-beta-glucosaminidase (NAG). The potential of these urines to inhibit crystal growth and agglomeration was also evaluated. After four weeks, the kidneys were screened by histology and radiography for the presence of CaOx crystals and the amount of kidney-associated oxalate was biochemically measured. Using 0.5 vol.% EG, only a part of the rats showed CaOx deposition in the renal cortex and/or medulla, without obvious differences between Wistar and Sprague-Dawley (SD) rats. If a dietary EG concentration of 0.75, 1.0, or 1.5 vol.% was used, the amount of kidney-associated oxalate was proportionally higher and CaOx crystal formation was consistently found in all rats. Most crystals were encountered in the cortex, whereas in the medulla and the papillary region, crystals were only occasionally detected. From these data, we conclude that in the chronic rat model, based on EG and vitamin D3, a consistent deposition of CaOx crystals is obtained using a EG concentration of at least 0.75%.
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PMID:Experimental nephrolithiasis in rats: the effect of ethylene glycol and vitamin D3 on the induction of renal calcium oxalate crystals. 981 34

Nephrolithiasis is a common disorder and a significant problem because of incidence, recurrence and severe consequences. Stone disease is a surgical as well as a medical problem. Major progress has been made recently in understanding the pathophysiological disturbances responsible for stone formation as well as in the techniques of stone removal. The introduction of extracorporeal shock wave lithotripsy has considerably reduced the need for surgery. Improvements in methods of kidney stone removal have not diminished the need for the application of an effective prophylactic program. The internist should take a complete history of stone events (number, composition, location and outcome of stone event), family history of stones, dietary habits (focusing on the consumption of animal protein, salt and dairy products), medications and physical examination. Radiopaque stones should be documented by plane X-ray films. Ultrasonography should be used to image calculi that are nonopaque, and to easily distinguish them from masses such as tumour or blood clot. Computed tomography is also an excellent method for imaging nonopaque renal calculi but higher cost and radiation exposure are disadvantages [2]. Crystallographic analysis is the essential diagnostic procedure. If available, previous stones should also be examined. "In stone disease, everything is measurement. What the laboratory cannot tell you, you will not know; what it tells you in error, you will not correct by using your instincts, your medical experience, or your art [3]". Reliable diagnostic protocols are available for the identification of different causes of stones. The complexity of protocols depend on the severity of nephrolithiasis. Patients with a single stone episode undergo simple protocol, and extensive detailed protocol is used for patients with recurrent stone disease, or patients at increased risk. Simple protocol, besides the already mentioned history of stone events, radiographic investigation and crystallographic analysis, includes serum urea, creatinine, uric acid, sodium, calcium, phosphorus and protein levels, urinary pH and volume, urine samples for culture and urinary calcium, uric acid, oxalate and citrate. Extensive metabolic evaluation includes simple protocol, determination of serum levels of alkaline phosphatase, parathyroid hormone, thyroxin, magnesium. A 24-h collection of urine specimen is analysed for urea, creatinine, uric acid, calcium, phosphate, sodium, magnesium, oxalate and citrate. Extensive protocol includes specialized evaluation tests [5]. Urinary acidification test is important for detecting distal renal tubular acidosis. Two 24-h urine specimens are collected while the patient is on the regular diet. The patient is then placed on a restricted diet (400 mg of calcium and 100 mEq of sodium) for a week, and another 24-h urine sample is collected. After that fasting and calcium load tests are performed (Sheme 1). Fasting urinary calcium is used to detect renal calcium leak, and calciuric response to oral calcium load provides an indirect measure of intestinal calcium absorption. Diagnostic criteria for major forms of stone disease [8] are presented in Table 1. There are some still unsolved questions: does time after passage of stones or urological intervention influence the frequency of urine abnormalities that can be detected; are there differences in 24-h urine composition between weekdays and weekends: what is the prevalence of the most important urinary risk factors of recurrent idiopathic calcium nephrolithiasis: do male patients differ from females with respect to urinary risk factors or recurrent idiopathic calcium nephrolithiasis? [7].
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PMID:[Functional evaluation in patients with kidney calculi]. 986 14

Calcium, in the form of regular food supplementation, can improve bone metabolism, but it can also increase the risk for renal calcium stones, and may aggravate pre-existing calcium urolithiasis. To study the first of these two aspects, ten healthy volunteers were given a conventional test meal (breakfast; calcium content 28 mg) with or without two dosages of calcium (as calcium-sodium citrate, CSC 1, 680 mg; CSC 2 1,360 mg), taken after an overnight 12 h fast. To study the latter aspect, patients with idiopathic recurrent calcium urolithiasis (ICU) received a balanced test meal of fixed composition, containing 1,000 mg calcium either as CSC (Meal + CSC3; n = 6) or as calcium gluconate (Mcal; n = 8). In normals, CSC induced a dose-dependent increasing intestinal absorption of calcium, and a decrease in oxalate absorption; in serum, CSC increased calcitonin and suppressed parathyroid hormone, but left unchanged the markers of bone turnover, serum osteocalcin and bone alkaline phosphatase. In urine, CSC decreased bone resorption markers (collagen crosslinks) and phosphaturia increased citrate, created signs of metabolic alkalosis, and inhibited several parameters of CaOx crystallization. In ICU, the CSC3 load failed to promote the crystallization of CaOx and calcium phosphate. It was concluded that CSC supplementation of a meal: (1) is well tolerated by healthy subjects and ICU patients, renders calcium highly available to bone, and prevents post-prandial oxaluria from rising; and, (2) is followed by the inhibition of crystallization of renal stone forming calcium-containing substances. Long-term studies aimed at evaluating the usefulness of CSC in preserving healthy bone, and in the metaphylaxis of renal stones would appear justified.
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PMID:Acute effects of calcium sodium citrate supplementation of a test meal on mineral homeostasis, oxalate, and calcium oxalate crystallization in the urine of healthy humans--preliminary results in patients with idiopathic calcium urolithiasis. 1042 48

To determine whether an "atherogenic" diet (excess of cholesterol and neutral fat) induces pathological calcification in various organs, including the kidney, and abnormal oxalate metabolism, 24 male Sprague-Dawley rats were fed either normal lab chow (controls, n = 12) or the cholesterol- and fat-rich experimental diet (CH-F, n = 12) for 111 +/- 3 days. CH-F rats developed dyslipidemia [high blood levels of triglycerides, total, low-density lipoprotein (LDL)-, very low-density lipoprotein (VLDL)-, high-density lipoprotein (HDL)-bound cholesterol, total phospholipids], elevated serum total alkaline phosphatase and lactate dehydrogenase (LDH) levels, in the absence of changes in overall renal function, extracellular mineral homeostasis [serum protein-corrected total calcium, magnesium, parathyroid hormone (PTH), 1,25-dihydroxyvitamin D (1,25(OH)2D)], plasma glycolate and oxalate levels. There was a redistribution of bone calcium and enhanced exchange of this within the extraosseous space, which was accompanied by significant bone calcium loss, but normal bone histomorphometry. Liver oxalate levels, if expressed per unit of defatted (DF) dry liver, were three times higher than in the controls. Urinary glycolate, oxalate, calcium and total protein excretion levels were elevated, the latter showing an excess of proteins > 100 kD and a deficit of proteins > 30-50 kD. Urinary calcium oxalate supersaturation was increased, and calcium phosphate supersaturation was unchanged. There were dramatically increased (by number, circumference, and area) renal calcium phosphate calcifications in the cortico-medullary region, but calcium oxalate deposits were not detectable. Electron microscopy (EM) and elemental analysis revealed intratubular calcium phosphate, apparently needle-like hydroxyapatite. Immunohistochemistry of renal tissue calcifications revealed co-localization of phospholipids and calcium phosphate. It is concluded that rats fed the CH-F diet exhibited: (1) a spectrum of metabolic abnormalities, the more prominent being dyslipidemia, hyperoxaluria, hypercalciuria, dysproteinuria, loss of bone calcium, and calcium phosphate nephrocalcinosis (NC); and (2) an interaction between calcium phosphate and phospholipids at the kidney level. The biological significance of these findings for the etiology of idiopathic calcium urolithiasis in humans is uncertain, but the presented animal model may be helpful when designing clinical studies.
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PMID:Nephrocalcinosis and hyperlipidemia in rats fed a cholesterol- and fat-rich diet: association with hyperoxaluria, altered kidney and bone minerals, and renal tissue phospholipid-calcium interaction. 1122 20

Urolithiasis, the process of formation of stones in the kidney and the urinary tract, is the major clinical manifestation of hyperoxaluria. Crystal deposition, as indicated by increased stone-forming constituents in urine, such as calcium, oxalate and uric acid, and decreased concentration of inhibitors, such as magnesium and glycosaminoglycans, was observed in pyridoxine-deficient hyperoxaluric rats. Renal tubular damage was indicated by increased excretion of enzymes such as alkaline phosphatase, lactate dehydrogenase, gamma-glutamyl transferase, beta-glucuronidase and N-acetyl glucosaminidase. Fibrinolytic activity was found to be reduced. Administration of pentacyclic triterpenes such as lupeol and its structural analogue betulin to hyperoxaluric rats minimised the tubular damage and reduced the markers of crystal deposition in the kidneys. In this connection, lupeol was found to be more effective than betulin.
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PMID:Control of urinary risk factors of stones by betulin and lupeol in experimental hyperoxaluria. 1144 2

Hyperoxaluria is one of the major risk factors for the formation of urinary calcium oxalate stones. Calcium oxalate crystals and their deposition have been implicated in inducing renal tubular damage. Lipoic acid (LA) and eicosapentaenoic acid (EPA) have been shown to ameliorate the changes associated with hyperoxaluria. This prompted us to investigate the nephroprotectant role of EPA-LA, a new derivative, in vivo in hyperoxaluric rats. Elevation in the levels of calcium, oxalate and phosphorus, the stone-forming constituents, were observed in calculogenic rats as a manifestation of crystal deposition. Tubular damage to the renal tissue was assessed byassaying the excretion of marker enzymes in the urine. Damage to the tubules was indicated by increased excretion of alkaline phosphatase (ALP), lactate dehydrogenase (LDH), gamma-glutamyl transferase (gamma-GT), beta-Glucuronidase (beta-GLU) and N-Acetyl beta-D glucosaminidase (NAG). Fibrinolytic activity was found to be reduced. Administration of EPA, LA and EPA-LA reduced the tubular damage and decreased the markers of crystal deposition markedly, which was substantiated by the reduction in weight of bladder stone formed. Our results highlight that EPA-LA is the most effective drug in inhibiting stone formation and mitigating renal damage caused by oxalate toxicity, thus confirming it as a nephroprotectant. Further work in this direction is warranted to establish the therapeutic effectiveness of this new derivative.
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PMID:Attenuation of oxalate-induced nephrotoxicity by eicosapentaenoate-lipoate (EPA-LA) derivative in experimental rat model. 1199 19

Investigations were carried out to evaluate the efficacy of the pentacyclic triterpene, lupeol and its ester, lupeol linoleate, against calcium oxalate urolithiasis in rats. Administration of a pyridoxine deficient diet containing 3% glycollic acid for 21 days led to increased excretion of stone forming constituents such as calcium, oxalate and uric acid. Crystal deposition and subsequent renal tubular damage resulted in increased excretion of the tubular enzymes alkaline phosphatase, lactate dehydrogenase, gamma glutamyl transferase, beta glucuronidase and N-acetyl glucosaminidase along with reduced fibrinolytic enzymes. A reduction in the urinary inhibitory factors magnesium and glycosaminoglycans was also observed. Treatment with lupeol and lupeol linoleate reduced the extent of tubular damage as evidenced from reduced enzymuria and minimized the excretion of stone forming constituents.
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PMID:Evaluation of the effect of triterpenes on urinary risk factors of stone formation in pyridoxine deficient hyperoxaluric rats. 1223 6

The effects of heparin, ethylenediaminetetraacetic acid (EDTA), sodium citrate and sodium fluoride/potassium oxalate on plasma biochemistry results in dogs were studied and compared with serum. Blood specimens from 10 apparently clinical healthy dogs were collected and placed in different tubes containing each anticoagulant tested. Differences in albumin, acetylcholinesterase, ionized calcium and potassium were found between serum and heparinized plasma. Most metabolites and enzymes did not show any variation, but significant decreases in electrolytes, alkaline phosphatase, acetylcholinesterase, bile acids, fructosamine and albumin were found when EDTA was used. Sodium citrate produced a 10-15% decrease in most metabolites and enzymes, possibly due to a sample dilution effect. Sodium fluoride/potassium oxalate produced haemolysis which may have influenced changes in some biochemical parameters.
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PMID:The effects of different anticoagulants on routine canine plasma biochemistry. 1508 Aug 79

Oxalate induced renal calculi formation and the associated renal injury is thought to be caused by free radical mediated mechanisms. An in vivo model was used to investigate the effect of phycocyanin (from Spirulina platensis), a known antioxidant, against calcium oxalate urolithiasis. Male Wistar rats were divided into four groups. Hyperoxaluria was induced in two of these groups by intraperitoneal infusion of sodium oxalate (70 mg/kg) and a pretreatment of phycocyanin (100 mg/kg) as a single oral dosage was given, 1h prior to sodium oxalate infusion. An untreated control and drug control (phycocyanin alone) were also included in the study. We observed that phycocyanin significantly controlled the early biochemical changes in calcium oxalate stone formation. The antiurolithic nature of the drug was evaluated by the assessment of urinary risk factors and light microscopic observation of urinary crystals. Renal tubular damage as divulged by urinary marker enzymes (alkaline phosphatase, acid phosphatase and gamma-glutamyl transferase) and histopathological observations such as decreased tubulointerstitial, tubular dilatation and mononuclear inflammatory cells, indicated that renal damage was minimised in drug-pretreated group. Oxalate levels (P < 0.001) and lipid peroxidation (P < 0.001) in kidney tissue were significantly controlled by drug pretreatment, suggesting the ability of phycocyanin to quench the free radicals, thereby preventing the lipid peroxidation mediated tissue damage and oxalate entry. This accounts for the prevention of CaOx stones. Thus, the present analysis revealed the antioxidant and antiurolithic potential of phycocyanin thereby projecting it as a promising therapeutic agent against renal cell injury associated kidney stone formation.
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PMID:Prophylactic role of phycocyanin: a study of oxalate mediated renal cell injury. 1529 40


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