Urinary Acid Phosphatase Research Articles

Urinary marker panels for aggressive prostate cancer detection

Majority of patients with indolent prostate cancer (PCa) can be managed with active surveillance. Therefore, finding biomarkers for classifying patients between indolent and aggressive PCa is essential. In this study, we investigated urinary marker panels composed of urinary glycopeptides and/or urinary prostate-specific antigen (PSA) for their clinical utility in distinguishing non-aggressive (Grade Group 1) from aggressive (Grade Group ≥ 2) PCa. Urinary glycopeptides acquired via data-independent acquisition mass spectrometry (DIA-MS) were quantitatively analyzed, where prostatic acid phosphatase (ACPP), clusterin (CLU), alpha-1-acid glycoprotein 1 (ORM1), and CD antigen 97 (CD97) were selected to be evaluated in various combinations with and without urinary PSA. Targeted parallel reaction monitoring (PRM) assays of the glycopeptides from urinary ACPP and CLU were investigated along with urinary PSA for the ability of aggressive PCa detection. The multi-urinary marker panels, combined via logistic regression, were statistically evaluated using bootstrap resampling and validated by an independent cohort. Majority of the multi-urinary marker panels (e.g., a panel consisted of ACPP, CLU, and Urinary PSA) achieved area under the curve (AUC) ranged from 0.70 to 0.85. Thus, multi-marker panels investigated in this study showed clinically meaningful results on aggressive PCa detection to separate Grade Group 1 from Grade Group 2 and above warranting further evaluation in clinical setting in future.

Peptiduria: a potential early predictor of diabetic kidney disease.

To protect the kidney effectively with medication in type 2 diabetics, it is crucial to identify such at-risk patients early for treatment. We investigated whether peptiduria precedes proteinuria (the earliest urinary marker in our model), and thereby serve as an early predictor of diabetic nephropathy. A longitudinal study was performed in a rat model of diabetic nephropathy. Peptides, defined as degradation products of proteins of < 13kD size, were quantified by a previously validated method using a combination of Lowry and Biorad protein assays. Peptides in urine were also confirmed by chromatographically separating low molecular weight fractions from urine and quantifying albumin fragments in these fractions by enzyme immunoassay. Also, the mechanism of peptiduria was addressed by measuring acid phosphatase, a marker of lysosomal activity, in urine and on kidney sections (histochemically). In rats with diabetic nephropathy, proteinuria occurred after 12weeks of diabetes, while peptiduria occurred as early as 2weeks after diabetes. Peptiduria was confirmed by showing that the chromatographically separated low molecular weight fractions of urine containing albumin fragments is in proportion to the level of peptiduria. The time course of peptiduria paralleled the increase in urinary acid phosphatase suggesting that the mechanism of early peptiduria could be due to upregulation of lysosomal enzyme activity in the tubules. Our results showing that peptiduria precedes proteinuria in diabetic nephropathy provide a compelling rationale to perform a prospective human clinical trial to investigate whether peptiduria can serve as an early predictor of diabetic nephropathy.

Porast nivoa mikroalbuminurije uz urinarne enzime kod diabetične bolesti bubrega

Background: Diabetic kidney disease (DKD) is a time progressive problem, give rise in uncontrolled Diabetics increasing risks for chronic kidney disease (CKD) and/or end-stage renal disease (ESRD). The vulnerability to renal dysfunction manifested with sudden glomerular hypofiltration associated with micro-to macroalbuminuria passing to renal failure. So that, screening of specific enzymes shifts, or urinary albumin may predict onset diabetic nephropathy. Objective: The assessment of urinary alkaline phosphatase (ALP), alanine aminopeptidase (AAP), acid phosphatase (ACP) and microalbuminuria (MAU) for type II diabetic patients. Patients and Methods: In this study,120 type II diabetic patients were compared to 90 healthy volunteers of matched age and sex in Al-Leith General Hospital, Al-Leith Kidney Unit (AKU), Al-Leith, Makkah area, KSA in which random urine samples were collected for testing of MAU, ALP, AAP, ACP and Cr. Results: Mean values of measured biomarkers in patient group for MAU, ALP, AAP, ACP and Cr were 51.92 mg/I, 41.55 U/L, 20.17 U/L, 570.10 U/L and 2.92 mg/dl VS in control group were 12.59 mg/I, 8.84 U/L, 6.94 U/L, 385.87U/L and 1.07 mg/dl respectively. Additionally, there were statistically positive correlation between AAP with MAU and ALP; ACP with MAU, ALP and AAP; Cr level with MAU, ALP, AAP and ACP; on the other hand, there were positive significant correlation between duration of diabetes with all studied markers. Conclusion: Using of MAU in addition to other urinary enzymes could be beneficial non-invasive indicators for renal deterioration in type II diabetics.

A single low dose of cadmium exposure induces benign prostate hyperplasia like condition in rat: A novel benign prostate hyperplasia rodent model.

Abnormal prostate growth is the most prevalent pathological sign in aged human males, as reflected by high incidence of benign prostate hyperplasia (BPH) and prostate cancer. In spite of the high prevalence, the etiology and pathophysiology of BPH is unclear due to the lack of any established rodent model for study. It has been demonstrated that the cadmium (Cd) mimics the activity of androgen or estrogen by interacting with the steroid hormone receptors in the prostate and elicits BPH, but the specific receptor which binds to Cd is still unknown. Our lab studies with BPH patients highlighted a strong co-relation between smokings with increased Cd content. Changes in the maximum urinary flow rate (Qmax) and prostatic acid phosphatase (PAP) level further supports that Cd can induce BPH like condition. Therefore, the present study was aimed to induce BPH like condition in rats by Cd administration. The dose of cadmium was standardized in an age- and time-dependent manner, which was further examined by prostate weight, histology, and PAP levels that elucidated the pathogenesis of BPH. Further to understand the molecular basis, steroid hormone receptor antagonist experiment was performed. Gene expression and immunohistochemistry data suggest that Cd induces hyperplasia like condition by activating the androgen receptor and estrogen receptor-α and suppresses the action of estrogen receptor-β. The experimental model used here is a cost effective, less time consuming and potentially valuable tool for investigating the respective functions of epithelial and stromal hormone receptors. The applicability of this model would be helpful in understanding the pathogenesis of BPH and its progression.

Induction of renal damage in rats by a diet deficient in antioxidants

Male albino rats. age 28 days, were fed a diet containing both vitamin E (10 g/kg) and selenium (5 mg/kg) or a diet lacking these antioxidants. Animals were examined for renal function after 4, 8, 12 and 16 wk on the respective diets. After 8 wk, animals on the deficient diet weighed less than controls (15%, p<0.01), and this became more pronounced by 16 weeks (25%, p<0.01). Expressed on a body weight basis, kidney wet weights did not differ between the two groups of animals. Urine volume increased in the animals fed the deficient diet at 8 weeks (66%, p<0.01) and this was maintained at 16 weeks (35%, p<0.01). Similar increases were observed for the rates of excretion of urinary total protein (77% elevation at 16 wk, p<0.01) and urinary acid phosphatase (51% elevation, p<0.01). At 16 wk, the specific activity of renal acid phosphatase in the animals given the deficient diet was reduced in cortex (57%, p<0.01) and medulla (20%, p<0.01), but not in papilla. These data indicate that dietary antioxidant deficiency causes progressive and pronounced renal damage.

Acid phosphatase levels of irrigant solution during transurethral prostatectomy

The acid phosphatase level of irrigant solution used during transurethral prostate resections was measured in 20 patients. The mean acid phosphatase of the irrigant solution was 45.3 IU/L (S.D. 50.7). The degree of elevation of irrigant acid phosphatase was related to the weight of tissue resected, the duration of the resection, and the total volume of irrigant used. A transient elevation of serum acid phosphatase occurred postoperatively which was associated with the level of urinary acid phosphatase elevation and the amount of absorbed irrigant solution based on changes in serum sodium.

Protection by selenium against gentamicin-induced acute renal damage in the rat.

Gentamicin has been shown to induce renal tubular damage in man and laboratory animals and to result in elevated urinary excretion of some enzymes associated with specific cell regions in the kidney. In the present investigation, the possible protective effect of selenium against gentamicin-induced renal damage was tested by measuring the urinary excretion of some enzymes in the presence and absence of selenium. Our results show that a prior subcutaneous injection of selenium to rats for two days followed by a simultaneous S.C. injection of gentamicin and selenium resulted in a marked reduction in the excretion of such biochemical systems as the urine volume, urinary proteins, alkaline and acid phosphatases, beta-glucuronidase, muramidase, and glutamate dehydrogenase. Renal functional studies revealed that selenium-treated rats suffered less adverse effects compared to rats treated with gentamicin alone. Urinary acid phosphatase, beta-glucuronidase and muramidase, the three lysosomal enzymes tested, appeared to respond most readily to protection by selenium.

The effect of cephaloridine on the stability of rat kidney lysosomes

The administration of cephaloridine to rats caused a decrease in the excretion of acid phosphatase into the urine. The antibiotic itself had no effect on urinary acid phosphatase and inhibitors or proteolytic enzymes were not present in the urine from treated rats. Cephaloridine may therefore be stabilizing the lysosomal membrane in vivo and experiments with isolated lysosomes confirm this hypothesis. The lysosomal integrity was followed by measuring the acid phosphatase activity and the light scattering properties of the particles. A good correlation was obtained between these parameters in the case of thermal disruption and progesterone induced lysis of the lysosomes and low concentrations of cephaloridine (0.1–1.0 mmol/l) protected the lysosomes against this form of damage.

Sex guilt, sexual arousal, and urinary acid phosphatase output

This study investigated the relationship between the personality variable sex guilt and a proposed physiological measure of sexual arousal (urinary acid phosphatase level). Urinary acid phosphatase levels of 43 male college students were assessed both basally and after exposure to 19 sexually themed slides. As predicted, sex guilt was inversely related to both basal acid phosphatase level and changes in acid phosphatase level upon exposure to the erotic stimuli. In addition, sex guilt scores were correlated with subjects' self-reported reactions to the erotic stimuli. The relationships obtained provided further construct validity evidence for the sex-guilt measure. Finally, the relationship between sexual arousal and urinary acid phosphatase level was explored. The data provided only partial validation for the proposed relationship between sexual arousal and urinary acid phosphatase output.

Urinary acid phosphatase as an auxiliary index of androgenic response

Urinary acid phosphatase as an auxiliary index of androgenic response

Altered lysosomal glycohydrolase activities in juvenile diabetes mellitus.

Studies have been carried out on activities of lysosomal beta-N-acetylhexosaminidase (hex), beta-galactosidase (beta-gal), alpha-glucosidase (alpha-glu), and acid phosphatase (AP) in serum and urine from patients with juvenile diabetes and matched controls. There is a large increase in blood and urinary hex activity (the former presenting three distinct patterns of abnormality), a moderate increase in urinary beta-gal, and a small increase in urinary alpha-glu activity, but no elevation of blood or urinary AP in the diabetics. Urinary alpha-glu activity in the diabetics shows striking inhibition by glucose, and this may reflect a similar phenomenon in vivo. Although glycohydrolase activities are elevated in patients with no detectable microangiopathy, more striking changes may be observed in patients with severe small-vessel disease. These alterations may be associated with increased glycoprotein catabolism in the diabetic, an area in need of further studies in the human and experimental diabetic animal.

Identification of Glycoproteins with One and with Two or More Binding Sites to Con A by Crossed Immuno‐Affinoelectrophoresis

Glycoproteins with one binding site and glycoproteins with two or more binding sites to concanavalin A may be identified by crossed immuno‐affinoelectrophoresis with free. and with immobilized concanavalin A. Human urinary acid phosphatase and human serum cholinesterase were demonstrated to be molecules with one and two or more binding sites to concanavalin A, respectively.

Urinary Acid Phosphatase Secretion Under Different Arousal Conditions

Urinary Acid Phosphatase Secretion Under Different Arousal Conditions

Urinary acid phosphatase secretion under different arousal conditions.

ABSTRACTSeventy‐three undergraduate males were randomly assigned to five different conditions, sexual, anxiety, aggressive, and laughter arousals and a control group, as a test of the hypothesis that urinary acid phosphatase is a specific indicator of sexual arousal. Pre‐ and post‐arousal urine samples were analyzed for the amount of urinary acid phosphatase (AP) present, and significant increases occurred only in the sexual arousal condition. Both general and specific elements of arousal as well as a possible link between sexual arousal and anxiety are discussed. These findings support earlier results of studies in this area.

Studies of human kidney and urine acid phosphatase. I. Biochemical characeristics and in vitro factors influencing measurement.

The human kidney is a comparatively rich source of the enzyme acid phosphatase; the highest activity is found in the glomeruli. Since glomerular damage might be reflected by excretion of large quantities of this enzyme into the urine, the present study was undertaken to determine the biochemical characteristics of renal acid phosphatase as it appears in human urine and to establish optimum assay conditions for quantitative measurement of urinary enzyme activity. Enzyme kinetics, including substrate concentration requirement, Km values, and incubationtime characteristics, were determined for renal and urinary acid phosphatase. Stability of enzyme activity during storage and the effect of activators and inhibitors of the enzyme were examined. The influence of acid phosphatase activity derived from sources other than the kidney on the measurement of renal enzyme activity in the urine had to be considered; therefore, the selective inhibitory effects of various compounds on acid phosphatase derived from human kidney, prostate, and red and white blood cells have been studied. Renal and prostatic acid phosphatase share similar biochemical features, particularly with regard to selective inhibition. It was not possible to inhibit the urinary acid phosphatase contributed by prostate without simultaneously strongly affecting renal acid phosphatase. On the other hand, a selective inhibition of the urinary acid phosphatase contributed by erythrocytes and partially that contributed by leukocytes could be obtained. Bacteriuria was considered as a further source of error. The results indicate that it may be possible to utilize the measurement of urinary acid phosphatase activity as an index of glomerular damage in children and adult females but not in adult males, because of the contribution of prostatic acid phosphatase.

Correlation of Serum and Urine Enzyme Activity in Patients with Acute Myocardial Infarction

Abstract A correlation was made between the urinary excretion of GOT, GPT, LDH, HBD, and acid and alkaline phosphatase and their serum activity in 18 suspected cases of myocardial infarction. The diagnoses were made by a cardiologist without knowledge of the enzyme assays. The study included 2 cases of nontransmural infarction; 5 cases that had not sustained an infarction served as controls. Elevations of serum GOT, LDH, and HBD were found in 10 of 11 cases of transmural infarction, GPT and acid phosphatase in 5, and alkaline phosphatase in 7. Elevations in serum acid phosphatase were also found in the control group, and perhaps were related to the anticoagulation therapy. Urinary GOT and GPT activity was variable. Urinary LDH and HBD were elevated in 6 of the transmural infarction cases, usually when serum LDH and HBD activity was decreasing. Urinary acid phosphatase activity was essentially normal; but urinary alkaline phosphatase increased in 10 of the transmural infarction cases, and the average value remained high for more than 5 weeks. The only index that was elevated in all cases of acute transmural infarction was L-phenylalanine inhibition of urinary alkaline phosphatase activity.

Correlation of activities of the phosphatase of the urine and serum of normal and cirrhotic persons

The urinary excretion of acid and alkaline phosphatase in normal and cirrhotic men was correlated with the serum activities of these enzymes. Both serum and urine alkaline phosphatases were frequently elevated in cirrhosis and related to the severity of the disease. In normal men there was an inverse correlation between the serum activity of alkaline phosphatase and its clearance, suggesting the serum as a source. The increased excretion in cirrhosis could be due to changes in renal function or to renal damage. The activity of serum acid phosphatase is relatively constant in normal men whereas the urinary excretion is variable. In patients with cirrhosis, the urinary acid phosphatase activity is less variable and is in the low range. It is unlikely that the serum and the urine acid phosphatases are from the same source.

Circadian variation of serum acid phosphatase in prostatic cancer

A circadian variation in total serum acid phosphatase was demonstrated in 5 patients with prostatic carcinoma using the method of Fishman and Lerner. Blood samples were drawn from a polyethylene catheter every hour for 25 hours. The cancer patients all had elevated serum enzyme concentrations and the nocturnal decrease was 25–50 per cent of the highest day-time value. The highest values were usually found from 9 A.M. to 3 P.M. and the lowest from 9 P.M. to 3 A.M. This circadian variation was entirely accounted for by variations in the prostatic (tartrate inhibitable) fraction. Orchiectomy did not obliterate the rhythmical variation. Urinary acid phosphatase did not have a circadian variation in a patient with a definite variation in serum enzyme concentration. Two normal patients did not have a readily detectable rhythm although a minor variation within the normal range would have been obscured by technical variations in the procedure which became important at low enzyme concentrations.

The effect of psychic-sexual stimulation on urinary and serum acid phosphatase and plasma nonesterified fatty acids.

In an attempt to develop a quantitative chemical measure of the intensity of sexual arousal a study was made of urinary acid phosphatase secretion rate and plasma acid phosphatase levels in young men, as influenced by the viewing of a sexually arousing moving picture. In a group of 17 subjects, 12 showed an increase in urinary acid phosphatase secretion rate, but, this effect was not correlated with subjective response (as evaluated by questionnaires), nor was the enzyme response prevented by concomitant feelings of disgust or disapproval. Plasma acid phosphatase concentrations, measured in 12 subjects, did not change. In a control group of married women, significant changes in urinary acid phosphatase were not observed. Incidental observations that sexual arousal was accompanied by an increase in plasma nonesterified fatty acids were also made.

Effect of storage in deep freeze upon activity of urinary acid phosphatase.

It has been reported that the acid phosphatase of serum is inactivated after several days at room temperature, or even in a refrigerator, but the activity may be preserved for periods ranging up to 112 days at —15 C. Similar findings were reported for the acid phosphatase of leukocytes. We also found that temperatures maintained in a deep-freeze prevent inactivation of the acid phosphatase in tissue extracts and fluid. However, while studying total and prostatic acid phosphatase in serum,' we observed that urine which was placed in a deep-freeze for 24 hours or longer seemed to lose considerable activity of acid phosphatase. Inasmuch as the excretion of urinary acid phosphatase has been studied in certain physiologic and pathologic states, the problem of proper preservation of urine is important. Therefore, we decided to study the extent of inactivation of urinary acid phosphatase under freezing conditions, and to attempt to define the mechanism through which the inactrvation occurred.