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PubMed1970

Distribution of prostaglandins in rabbit kidney.

Three prostaglandins (PGE(2), PGF(2alpha) and PGA(2)) are present in rabbit kidney medulla. An acidic lipid extract (0.165g) obtained from 2kg of frozen rabbit kidney cortex was separated by silicic acid chromatography to yield eluates containing fatty acids, possible non-polar prostaglandin metabolites, PGA, PGE and PGF compounds. Ultraviolet spectra of the eluates before and after treatment with sodium hydroxide did not yield chromophores typical of any known prostaglandins or related metabolites. By using more sensitive bioassay procedures (contraction of rabbit duodenum) weak activity equivalent to 60mug of PGE(2) and 10mug of PGF(2alpha) was detected in the PGE and PGF eluates respectively. Extraction and bioassay of fresh kidney cortex revealed no prostaglandin-like activity. Attempts to biosynthesize prostaglandins in fresh homogenates of rabbit kidney cortex from endogenous precursors and from added arachidonic acid were unsuccessful. When freshly prepared homogenates of rabbit kidney cortex were incubated with added PGE(1) no evidence of enzymic breakdown was obtained. It is concluded that rabbit kidney prostaglandins are present predominantly in the medulla and there are no cortical mechanisms for their biosynthesis or inactivation under normal conditions.

Animals↗
PubMed1981

Characterization of the proteinuria induced by prolonged oral administration of cadmium in female rats.

Female Sprague-Dawley rats were given 200 ppm cadmium (Cd) in the drinking water for 11 months. Total proteinuria and the concentrations of Cd in blood, urine, liver and kidney cortex were determined monthly. The proteinuria was characterized by Sephadex G-75 chromatography and by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. From the 8th month of treatment, the Cd concentration in the kidney cortex levels off at a value of about 250 microgram/g wet wt and this phenomenon coincides with the occurrence of proteinuria. The proteinuria was characterized by an increased urinary excretion of high molecular weight (HMW) proteins, particularly gamma-globulins. Aminoaciduria also increased which suggests the existence of a slight tubular dysfunction. The renal dysfunction induced by chronic oral administration of Cd seems different from that observed in a previous study in which Cd was administered by the i.p. route (1 mg Cd/kg, 5 times a week for 2 months). For the same level of Cd in the kidney cortex the proteinuria induced by i.p. injection of Cd was usually of mixed type and in some cases of the tubular type. The development of this proteinuria was coincident with the levelling off of Cd concentration in the kidney cortex and in the liver. The saturation of liver by Cd is very likely at the origin of he extensive tubular lesion and of the mixed type proteinuria observed in the i.p. experiment. These results demonstrate the importance of mode of Cd administration on the nature of the Cd-induced proteinuria in animal. They support also our proposal that both low and HMW proteins should be determined in urine for the early detection of renal damage occurring in man chronically exposed to cadmium.

Administration, Oral↗
PubMed2001

Suppressive role of endogenous regucalcin in the regulation of protein phosphatase activity in rat renal cortex cytosol.

The role of endogenous regucalcin, which is a regulatory protein of calcium signaling, in the regulation of protein phosphatase activity in the cytosol of rat renal cortex was investigated. Protein phosphatase activity toward phosphotyrosine, phosphoserine, and phosphothreonine was found in the cytosol of kidney cortex. The addition of regucalcin (50-250 nM) in the enzyme reaction mixture caused a significant decrease in protein phosphatase activity toward three phosphoamino acids. The effect of calcium (25 microM) and calmodulin (2.5 microg/ml) in increasing protein phosphatase activity toward three phosphoamino acids was significantly decreased by the addition of regucalcin (100 nM). Protein phosphatase activity toward three phosphoamino acids was significantly increased in the presence of anti-regucalcin monoclonal antibody (10-50 ng/ml) in the enzyme reaction mixture. The effect of antibody (25 ng/ml) in increasing the enzyme activity was significantly inhibited by cyclosporin A (10(-5) M) or vanadate (10(-5) M). Regucalcin in the kidney cortex cytosol was clearly decreased by the administration of saline (0.9% NaCl) for seven days in rats. Protein phosphatase activity toward three phosphoamino acids was significantly decreased by saline administration. The effect of anti-regucalcin antibody (25 ng/ml) in increasing protein phosphatase activity toward three phosphoamino acids was not seen in the renal cortex cytocol of saline-administered rats. The present study demonstrates that endogenous regucalcin plays a suppressive role in the regulation of protein phosphatase activity in the cytoplasm of rat kidney cortex.

Animals↗
PubMed2002

Vasodilatory N-methyl-D-aspartate receptors are constitutively expressed in rat kidney.

N-methyl-D-aspartate receptor (NMDA-R) is an amino acid receptor and membrane calcium channel. NMDA-R is activated by binding of coagonists, L-glutamine and L-glycine. In the brain, calcium entry via NMDA-R activates type I nitric oxide synthase (NOS I). The kidney also contains NOS I and vasodilates in response to L-glycine. In this study, NMDA-R mRNA was demonstrated in rat kidney cortex by reverse transcriptase-PCR and cDNA sequencing. NMDA-R protein was demonstrated in kidney cortex by immunoblotting. To study the functional role of renal NMDA-R, renal hemodynamic effects of NMDA-R inhibition were assessed in rats using a blocker of the NMDA calcium channel (75 mg/kg MK-801 intraperitoneally) or an inhibitor of glycine binding to NMDA-R (30 mg/kg 5,7-dichlorokynurenic acid intraperitoneally). Renal blood flow was measured by perivascular pulse Doppler. GFR was measured by 3H-inulin clearance. Measurements were made before and during glycine infusion. Both NMDA-R antagonists caused renal vasoconstriction and attenuated the renal vasodilatory response to glycine infusion. These effects were not mediated by the renal nerves. The glycine response was not inhibited by aortic snare used to mimic the effects of NMDA-R inhibitors on basal renal blood flow. NMDA-R are expressed in kidney cortex, where they exert a tonic vasodilatory influence and may account for the vasodilatory response to glycine infusion.

Analysis of Variance↗
PubMed2002

Trace elements distribution in renal cell carcinoma depending on stage of disease.

OBJECTIVES: The aim of this study was to identify those trace elements which can be used to distinguish between normal and malignant tissue in renal cell cancer (RCC) kidney and to assess changes in trace elements concentration in tissue with progressing malignant disease. METHODS: In case control study, 36 cases of RCC were analyzed by Synchrotron Radiation Induced X-ray Emission (SRIXE) in order to establish the concentration of 19 elements. Patients with RCC were examined to obtain staging of disease after radical nephrectomy, which was performed in each case. Results were compared with 15 control kidney cortex tissue obtained during autopsy in which cause of death was trauma. RESULTS: The most relevant decrease was detected in Cd content: from 81 +/- 39.2 ppm in normal control samples to 16.6 +/- 22.2 ppm concentration in RCC. We found that the concentrations of Ti, Pb and Rb were also lower in RCC tissue. On the other hand, the RCC tissue was rich in iron and zirconium. With the progress of malignant disease, assessed by TNM (UICC 1997) scale, lower concentration of S and higher concentration of Ca in both RCC and neoplastic kidney cortex can be seen. The same tendency is observed in Zn and Se concentrations. Cadmium shows raising concentration with progress of RCC only in cortex of neoplastic kidney. In all cases it was shown that the relatively high tissue concentration of iron in both investigated tissues is decreasing with the progress of disease. The zirconium has shown raising tissue concentration in advanced disease. CONCLUSION: Trace elements concentration is different in malignant tissue and surrounding macroscopically unchanged kidney cortex. Progress of the disease is connected with changes in trace elements concentration. This may reflect different biology of compared tissue with potential practical implication.

Aged↗
PubMed1998

cDNA cloning and expression of a novel family of enzymes with calcium-independent phospholipase A2 and lysophospholipase activities.

Previous studies have suggested that activation of calcium-independent PLA2 (CaIPLA2) is an early event in cell death after hypoxic injury in proximal tubule cells. An approximately 28-kD CaIPLA2 with preferential activity toward plasmalogen phospholipids has been recently purified from rabbit kidney cortex (D. Portilla and G. Dai, J Biol Chem 271, 15,451-15,457, 1996). Their report describes the cloning of a full-length rat cDNA encoding CaIPLA2, using sequences derived from the purified rabbit kidney cortex enzyme. In addition, cDNA from rabbit kidney that encode the rabbit homologue of the enzyme and a closely related isoform were isolated. The rat cDNA is predicted to encode an approximately 24-kD protein, and each cDNA contains the sequence G-F-S-Q-G, which fits the active site consensus sequence G-X-S-X-G of carboxylesterases. Several lines of evidence (DNA sequence comparison, Southern blot analysis, and examination of the expressed sequence tag database) show that CaIPLA2 enzymes are encoded by a multigene family in rats, mice, rabbits, and humans. Northern analysis of various tissues from the rat indicated that the CaIPLA2 gene is ubiquitously expressed, with highest mRNA abundance observed in the kidney and small intestine. The rat CaIPLA2 cDNA, when expressed in a baculovirus expression system, and the purified rabbit kidney cortex protein exhibit both CaIPLA2 and lysophospholipase activities. The cloned CaIPLA2 cDNA are expected to aid in understanding the role of CaIPLA2 in cell death after hypoxic/ischemic cell injury.

Amino Acid Sequence↗
PubMed1994

Origin of chlortetracycline in pig tissue.

Violative chlortetracycline (CTC) residues in excess of the maximum residue limit (MRL) have been identified in 0.9% of all pigs tested at slaughter in Northern Ireland. Three experiments were carried out to investigate the possible reasons. In Experiment 1, pigs were fed CTC at therapeutic levels (300 mg kg-1 head-1 d-1) for 7 days and were slaughtered at day 0, 2, 4, 6, 8 and 10 following CTC withdrawal. Muscle, liver and kidney cortex and medulla samples were analysed for CTC residues by using high-performance liquid chromatography (HPLC). In all tissues, residues were less than the MRL from day 2 onwards. Mean CTC concentrations in kidney cortex were greater than medulla concentrations (p < 0.05). In Experiment 2, feed spiked with a sub-therapeutic dose of CTC (40 mg kg-1) was fed to six pigs that were slaughtered after 4, 8 and 12 days of medication. Violative CTC residues were not detected. In Experiment 3, short term supra-therapeutic administration was examined. Eight pigs received 500 mg kg-1 CTC head-1 d-1 for 1 or 2 days and were killed in pairs, 24 and 48 h following the final medicated feed. Violative levels were detected in both groups after 24 h only. It is concluded that: firstly, recommended CTC withdrawal periods are sufficient to avoid violative carcass residues; secondly, violative residues do not arise from sub-therapeutic dosing but can arise from supra-therapeutic dosing which could occur with inadequately mixed feed; and thirdly, the difference in kidney cortex and medullary CTC concentrations is significant from a regulatory perspective.

Animal Feed↗
PubMed1997

Lead-induced hypertension: interplay of nitric oxide and reactive oxygen species.

An elevation of mean blood pressure was found in rats treated with low lead (0.01% lead acetate) for 3 months, as contrasted to paired Sprague-Dawley control rats. In these rats, measurement of plasma and urine endothelins-1 and -3 revealed that plasma concentration and urinary excretion of endothelin-3 increased significantly after 3 months (plasma: lead group, 31.8+/-2.2, versus controls, 23.0+1.7 pg/mL, P<.001; urinary excretion: lead group, 46.6+11.7, versus controls, 35.6+6.7 pg/24 h, P<.05), whereas endothelin-1 was unaffected. Plasma and urinary nitric oxide (NO) and cyclic GMP concentrations were not significantly changed. However, assay of plasma and kidney cortex malondialdehyde by high-pressure liquid chromatography, as a measure of reactive oxygen species, was elevated in lead-treated rats compared with that in control rats (plasma: lead group, 4.74+1.27, versus controls, 2.14+.49 micromol/L, P<.001; kidney cortex: lead group, 28.75+3.46, versus controls, 16.38+2.37 nmol/g wet weight, P<.001). There was increased NO synthase activity in lead-treated rat brain cortex and cerebellum. In lead-treated rat kidney cortex, the endothelial constitutive NO synthase protein mass was unaffected, whereas the inducible NO synthase protein mass was increased. These data suggest a balance between increased NO synthesis and degradation (by reactive oxygen species) in lead-treated rats, which results in normal levels of NO. Thus, the hypertension may be related to an increase in the pressure substances, endothelin-3 and reactive oxygen species, rather than to an absolute decrease in nitric NO.

Animals↗
PubMed1988

Presence of dopamine-dependent adenylate cyclase activity in human renal cortex.

The effects of dopamine (DA) and of two selective DA DA1 agonists (SKF 38393 and SKF 82526) on adenylate cyclase activity were studied with human kidney cortex membrane preparations. DA elicited a dose-related stimulation of adenylate cyclase activity with an EC50 of 60 microM. The selective DA DA1 antagonist SCH 23390 behaved as a competitive antagonist, shifting the dose-response curve to the right. The non-selective beta-adrenoceptor antagonist (-)-propranolol did not affect the EC50 of the dose-response curve to DA but attenuated the maximal stimulatory effect of DA at concentrations higher than 100 microM. (+)-Sulpiride inhibited DA-induced adenylate cyclase stimulation in a dose-dependent manner with an IC50 of 4.6 X 10(-8) M but (-)-sulpiride was without effect. Both SKF 38393 and SKF 82526 stimulated the adenylate cyclase activity of human kidney cortex; this effect was completely antagonized by SCH 23390. Our results, demonstrating the presence of DA-sensitive adenylate cyclase activity, strongly suggest the presence of a DA receptor of the DA1 subtype in human kidney cortex.

Adenylyl Cyclases↗
PubMed2000

Distribution of rhodanese in different parts of the urogenital systems of sheep at pre- and post-natal stages.

The enzyme rhodanese (thiosulfate:cyanide sulfurtransferase) is a ubiquitous enzyme present in all living organisms, from bacteria to humans and plays a central role in cyanide detoxification. The purpose of this investigation is to determine and compare rhodanese activity in different parts of urogenital systems of male and female sheep fetuses at 2.5, 3, 3.5, 4, 4.5, and 5 months of age. The highest activity of rhodanese in male fetus was in kidney cortex, followed by medulla of the kidney. No significant difference was observed in other organs. In female fetus, the highest activity was in kidney cortex followed by oviduct and medulla of kidney. The enzyme activity of tissues increased with age. There was no significant difference (P > 0.05) between male and female fetuses in levels of rhodanese activity of different tissues except in urinary bladder at 2.5 and 3 months and in urethra at 4.5 months of age. The results of this study might indicate the involvement of rhodanese in cyanide detoxification in tissues which are more exposed to cyanide. On the other hand, rhodanese might perform other functions which are specific in these tissues.

Animals↗
PubMed1984

In vitro rates of oxidation and gluconeogenesis from L(+)- and D(-)lactate in bovine tissues.

Slices of bovine kidney cortex, liver, heart and sternomandibularis muscle actively metabolized D- and L-lactate. Rates of D-lactate oxidation were greatest in kidney cortex followed by heart and liver with muscle exhibiting the lowest rates. L-lactate oxidation was greatest in kidney cortex followed by heart with liver and muscle exhibiting similar rates. Rates of oxidation of gluconeogenesis were similar for D- and L-lactate at 0.1 mm lactate but D utilization, as a percent of L, decreased as substrate concentrations increased to 50 mM. Bovine tissues appear to possess significant potential for D(-)lactate utilization. Estimates of this and possible interactions are discussed.

Animals↗
PubMed1975

Stimulation of renal gluconeogenesis by L-alanine and AIB.

L-alanine as well as AIB have been shown to stimulate gluconeogenesis in isolated kidney cortex tubules in a catalytic way. The data reported are consistent with the view, that the stimulation of renal gluconeogenesis by L-alanine and AIB is due to an inhibition of glycolysis at the level of the pyruvate kinase reaction. In the light of results of Carminatti et al. [8], showing that in kidney cortex 70-80% of total pyruvate kinase activity is represented by a type which is insensitive to inhibition by ATP but sensitive to inhibition by alanine, it appears conceivable also from our results, that alanine counteracted by FDP might contribute to the regulation of pyruvate kinase acti-ity and consequently thereby gluconeogenesis in kidney cortex.

Alanine↗
PubMed1993

Preparation and biological characteristics of 99mTc-diol a renal agent.

The present work concerns the production of 1,2-dihydroxypropyl-1-phosphonic acid (diol) by acid hydrolysis of (-cis) 1,2-epoxypropylphosphonic acid (phosphomycin), and its formulation as a kit easily labeled with [99mTc]pertechnetate. Biodistribution studies and whole-body autoradiographies in mice show that 99mTc-diol has a specific affinity for the kidneys: it is rapidly cleared from the blood and excreted in urine (12.09 +/- 6.40% ID are excreted in urine at 5 min and 70.81 +/- 2.41% ID at 30 min post-injection). Part of the injected activity remains in the kidney cortex sufficiently long to permit kidney imaging (5.66 +/- 0.91% ID is still in kidneys 1 h post-injection). In comparison with other agents which also localize in the kidney cortex, such as 99mTc-DMSA and 99mTc-glucoheptonate (99mTc-GHA), the main differences are the following: the peak of renal activity is reached early in the 5 min post-injection period for 99mTc-diol, only at about 10 min post-injection for 99mTc-GHA and after 3 h post-injection for 99mTc-DMSA. The uptake of 99mTc-diol by other organs, especially by bones, is much smaller than in the case of 99mTc-DMSA (1.25 +/- 0.11% ID of 99mTc-diol compared to 11.31 +/- 1.17% ID of 99mTc-DMSA, 1 h post-injection). Unlike 99mTc-DMSA, the biodistribution of 99mTc-diol is not significantly influenced by acid-base imbalance, in addition, its renal uptake decreases in the presence of probenecid whereas its urinary excretion increases.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Imbalance↗
PubMed2000

Mercury, selenium, and cadmium in human autopsy samples from Idrija residents and mercury mine workers.

Total Hg and Se concentrations were determined in autopsy samples of retired Idrija mercury mine workers, Idrija residents living in a Hg-contaminated environment, and a control group with no known Hg exposure from the environment. In selected samples we also checked the presence of MeHg. The highest Hg concentrations were found in endocrine glands and kidney cortex, regardless of the group. MeHg contributed only to a negligible degree to the total mercury concentrations in all analyzed samples. In the Hg-exposed groups the coaccumulation and retention of mercury and selenium was confirmed. Selenium coaccumulation with a Hg/Se molar ratio near 1 or higher was notable only in those tissue samples (thyroid, pituitary, kidney cortex, nucleus dentatus) where the mercury concentrations were >1 microg/g. After tissue separation of such samples the majority of these elements were found in the cell pellet. Because the general population is continuously exposed to Cd and possibly also to Pb from water, food, and/or air, in some samples the levels of these elements were also followed. In all examined control tissue samples the average values of Cd (kidney cortex, thyroid, hippocampus, cortex cerebellum, nucleus dentatus) and Pb (thyroid, hippocampus) exceeded the average values of Hg. Cd concentrations were the highest, particularly in kidney cortex and thyroids (microg/g), but no relationship between Cd and Se concentration was evident at the tissue level. Regarding the results in the control group, it is debatable which element is the more hazardous for the general population as concerns neurotoxicity.

Adult↗
PubMed1995

Mechanism of citrinin-induced dysfunction of mitochondria. IV--Effect on Ca2+ transport.

The effect of citrinin on Ca2+ transport was studied in isolated kidney cortex and liver mitochondria, and baby hamster kidney cultured cells. The mycotoxin significantly inhibited the activity of 2-oxoglutarate and pyruvate dehydrogenases in both kidney cortex and liver mitochondria. Citrinin promoted a decrease in the velocity and in the total capacity of Ca2+ uptake, in both mitochondria. Apparently, citrinin acts by a mechanism similar to ruthenium red. In intact cultured cells, citrinin also had a preferential effect on mitochondrial Ca2+ fluxes. Citrinin promoted a marked decrease in the Ca2+ level in the mitochondrial matrix, whereas that of the extramitochondiral fraction became less affected. All the observed effects were dependent on the citrinin concentration.

Animals↗