Plasma ribonuclease uptake by rat kidney cortex.
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Animals↗
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The interdependence between high cadmium content of horse kidney cortex and the false positive kidney test for the detection of antibiotic residues at meat inspection.
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Absorption↗
Metabolism of acetaldehyde in human and baboon renal cortex. Ethanol synthesis by isolated baboon kidney-cortex tubules.
Acetaldehyde (1-20 mM) was metabolized at high rates and in a dose-dependent manner in isolated human and baboon kidney-cortex tubules. Acetaldehyde removal was accompanied by a large accumulation of acetate in both human and baboon tubules. By contrast, a large synthesis of ethanol was observed only in baboon tubules. Consistent with the latter finding, ethanol was found to be metabolized at significant rates in baboon but not human tubules. In the tubules from both species, a significant fraction of the acetaldehyde removed was also completely oxidized to CO2 and H2O. These results suggest that, in both man and baboon, the kidneys participate in the in vivo metabolism of acetaldehyde; they also suggest that, in contrast with the human kidneys, the baboon kidneys contribute to the detoxication of circulating ethanol.
Acetaldehyde↗
The fuel of respiration of rat kidney cortex.
1. In kidney-cortex slices from the well-fed rat, glucose (5mm) supplied 25-30% of the respiratory fuel; in the starved state, the corresponding value was 10%. These results are based on measurements of the net uptake of glucose and of the specific radioactivity of labelled carbon dioxide formed in the presence of [U-(14)C]-glucose. 2. Added acetoacetate (5mm) or butyrate (10mm) provided up to 80%, and added oleate (2mm) up to 50% of the fuel of respiration. The oxidation of endogenous substrates was suppressed correspondingly. 3. More [U-(14)C]oleate was removed by the tissue than could be oxidized by the amount of oxygen taken up; less than 25% of the oleate removed was converted into respiratory carbon dioxide and about two-thirds was incorporated into the tissue lipids. The rate of oleate incorporation into the neutral-lipid fraction was calculated to be equivalent to the rate of oxidation of endogenous fat, which provided the chief remaining fuel. 4. The contribution of endogenous substrates to the respiration (50%) in the presence of added oleate is taken to reflect either a high turnover rate of the endogenous neutral lipids (approx. half-life 2.5hr.) or a raised rate of lipolysis caused by the experimental conditions in vitro. 5. Added l-alpha-glycerophosphate (2.5mm) increased oleate incorporation into the neutral-lipid fraction by up to 40% (i.e. caused a net synthesis of triglyceride). 6. Lactate (2.5mm) added as sole substrate supplied 30% of the respiratory fuel, but with added oleate (2mm) lactate was converted quantitatively into glucose. Oleate stimulated the rate of gluconeogenesis from lactate by 45%. 7. The oxidation of both long-chain and short-chain even-numbered fatty acids was accompanied by ketone-body formation. Ketone-body synthesis from oleate, but not from butyrate, increased six- to seven-fold after 48hr. of starvation. The maximum rates of renal ketogenesis (80mumoles/hr./g. dry wt., with butyrate) were about 20% of the maximum rates observed in the liver (on a weight-for-weight basis) and accounted for, at most, 35% of the fatty acid removed. 8. dl-Carnitine (1.0mm) had no effect on the rates of uptake of acetate, butyrate or oleate or on the rate of radioactive carbon dioxide formation from [U-(14)C]oleate, but increased ketone-body formation from oleate by more than 100%. Ketone-body formation from butyrate was not increased. 9. There is evidence supporting the assumption that there are cells in which gluconeogenesis and ketogenesis occur together, characterized by equal labelling of [U-(14)C]oleate and the ketone bodies formed, and other cells that oxidize fat and do not form ketone bodies. 10. Inhibitory effects of unlabelled acetoacetate on the oxidation of [1-(14)C]butyrate and of unlabelled butyrate on [4-(14)C]acetoacetate oxidation show that fatty acids and ketone bodies compete as fuels on the basis of their relative concentrations. 11. The pathway of ketogenesis in renal cortex must differ from that of the liver, as beta-hydroxy-beta-methylglutaryl-CoA synthetase is virtually absent from the kidney. In contrast with the liver the kidney possesses 3-oxo acid CoA-transferase (EC 2.8.3.5), and the ready reversibility of this reaction and that of thiolase (EC 2.3.1.9) provide a mechanism for ketone-body formation from acetyl-CoA. This mechanism may apply to extrahepatic tissues generally, with the possible exception of the epithelium of the rumen and intestines.
Acetoacetates↗
Stimulatory effect of calcium administration on regucalcin mRNA expression is attenuated in the kidney cortex of rats ingested with saline.
The expression of calcium-binding protein regucalcin mRNA in the kidney cortex of rats ingested with saline was investigated. The alteration in regucalcin mRNA levels was analyzed by Northern blotting using liver regucalcin complementary DNA (0.9 kb of open reading frame). Rats were freely given saline as drinking water for 7 days. Regucalcin mRNA levels in the kidney cortex were suppressed by saline ingestion. When calcium chloride (10 mg Ca/100 g body weight) was intraperitoneally administered to rats ingested with saline for 7 days, the effect of calcium administration to increase regucalcin mRNA levels was weakened by saline ingestion. Such effect was also seen by the administration of 2.5 and 5 mg Ca/100 g. Regucalcin mRNA levels in the kidney cortex of spontaneous hypertensive rats (SHR) were not appreciably increased by the administration of calcium (10 mg/100 g). Meanwhile, calcium content in the kidney cortex was significantly elevated by the administration of calcium (10 mg/100 g) to normal rats. This increase was weakened in saline-ingested rats. Moreover, Ca2+/calmodulin-dependent protein kinase activity in the cytosol of kidney cortex was significantly decreased by saline ingestion. These results suggest the possibility that saline ingestion-induced suppression of regucalcin mRNA expression in the kidney cortex is partly involved in the attenuation of Ca2+ signalling.
Animals↗
Involvement of nuclear factor-1 (NF1) binding motif in the regucalcin gene expression of rat kidney cortex: the expression is suppressed by cisplatin administration.
The binding of nuclear factor on the promoter region of the regucalcin gene and the expression of regucalcin in the kidney cortex of rats was investigated. Nuclear extracts from kidney cortex were used for oligonucleotide competition gel mobility shift assay. An oligonucleotide between position -523 and -506 in the 5'-flanking region of the rat regucalcin gene, which contains a nuclear factor 1 (NF1) consensus motif TTGGC(N)6CC, competed with the probe for the binding of the nuclear protein from kidney cortex. The mutation of TTGGC in the consensus sequence caused an inhibition of the binding of nuclear factors. The binding of nuclear factor on the 5'-flanking region was clearly reduced in the kidney cortex obtained at 1, 2, and 3 days after a single intraperitoneal administration of cisplatin (1.0 mg/100 g body wt) to rats. Moreover, cisplatin administration caused a remarkable decrease in regucalcin mRNA levels and regucalcin concentration in the kidney cortex. Also, serum regucalcin concentration was significantly decreased by cisplatin administration. Meanwhile, serum urea nitrogen concentration was markedly elevated by cisplatin administration. The present study demonstrates that the specific nuclear factor binds to the NF1-like sequence in the promotor region of regucalcin gene in the kidney cortex of rats, and that the nuclear factor binding and regucalcin expression are suppressed by cisplatin administration.
Amino Acid Motifs↗
[Low temperature and cryoprotectant effect on oxygen uptake in rat kidney cortex homogenates].
Respiration and oxidative phosphorylation of the rat kidney cortex mitochondria are studied as affected by low temperatures and cryoprotectants. There is no change in respiration in state 2 during freezing and thawing of the rat kidney cortex slices both in case of using the succinate oxidation substrate and alpha-ketoglutarate. Respiration in state 3 is inhibited in the medium with alpha-ketoglutarate during freezing under protection of polyethylene oxide-100 (PEO-100) and glycerol, and does not significantly change in case of using dimethyl sulphoxide (DMSO). The effectiveness of cryoprotectants used in the experiments reduces in the following sequence: DMSO--glycerol--PEO-100. Preservation of the main mitochondria function, ATP synthesis, is shown to be possible for the kidney cortex slices exposed to freezing and thawing.
Adenosine Triphosphate↗
Fatty acid hydroxylation in rat kidney cortex microsomes.
Rat kidney microsomes have been found to catalyze the hydroxylation of medium-chained fatty acids to the omega- and (omego-1)-hydroxy derivatives. This reaction, which requires NADPH and molecular oxygen, is a function of monooxygenase system present in the kidney microsomes, containing NADPH-cytochrome c reductase and cytochrome P-450K. NADH is about half as effective as an electron donor as NADPH and there is an additive effect in the presence of both nucleotides. Cytochrome P-450K absorbs light maximally at 452-3 nm, when it is reduced and bound to carbon monoxide. The extinction coefficient of this complex is 91 mM(-1) cm(-1). Electrons from NADPH are transferred to cytochrome P-450K via the NADPH-cytochrome c reductase. The reduction rate of cytochrome P-450K is stimulated by added fatty acids and the reduction kinetics reveal the presence of endogenous substrates bound to cytochrome P-450K. Both cytochrome P-450K concentration and fatty acid hydroxylation activity in kidney microsomes are increased by starvation. On the other hand, phenobarbital treatment of the rats has no effect on either the hemoprotein or the overall hydroxylation reaction and 3,4-benzpyrene administration induces a new species of cytochrome P-450K not involved in fatty acid hydroxylation. Cytochrome P-450K shows, in contrast to liver P-450, high substrate specificity. The only substances forming enzyme-substrate complexes with cytochrome P-450K are the medium-chained fatty acids and certain derivatives of these acids. The chemical requirements for substrate binding include a carbon chain of medium length and at the end of the chain a carbonyl group and a free electron pair on a neighbouring atom. The distance between the binding site for the carbonyl group and the active oxygen is suggested to be in the order of 16 A. This distance fixes the ratio of omega- and (omega-1)-hydroxylated products formed from a certain fatty acid by the single species of cytochrome P-450K involved. The membrane microenvironment seems also to be of importance for the substrate specificity of cytochrome P-450K, since removal of the cytochrome from the membrane lowers its binding specificity to some extent. A comparison between the liver and kidney cytochrome P-450 systems suggests that the kidney cytochrome P-450K system is specialized for fatty acid hydroxylation.
Animals↗
Effect of cyclosporin A and different vehicles on ATP production in mitochondria isolated from the rat kidney cortex.
Isolated rat kidney mitochondria were exposed in vitro to cyclosporin A and three different vehicles, ethanol, DMSO and cremophor. Spontaneous ATP production and oxidative phosphorylation were measured with a bioluminometric method. Both ethanol and cremophor caused a slight (4-7%) decrease in spontaneous ATP production, and also cyclosporin A itself had a minimal effect. On the other hand DMSO had an opposite effect, causing an increase of about 20%. Cyclosporin A showed a dose dependent inhibition of oxidative phosphorylation, being most pronounced when dissolved in ethanol. Cremophor, the castor oil used in commercial preparations caused per se almost a 40% inhibition of the oxidative phosphorylation.
Adenosine Triphosphate↗
Steroid hormonal regulation of calcium-binding protein regucalcin mRNA expression in the kidney cortex of rats.
The effect of various steroid hormones on the expression of calcium-binding protein regucalcin mRNA in the kidney cortex of rats was investigated. The change of regucalcin mRNA levels was analyzed by Northern blotting using rat liver regucalcin complementary DNA (0.9 kb of open-reading frame). Regucalcin mRNA was expressed in the kidney cortex but not the medulla. Rats received a single subcutaneous administration of steroid; the animals were sacrificed 60 min after the treatment of aldosterone (2.5, 5.0 and 10 micrograms/100 g body weight) or 6 h after the treatment of estrogen (17 beta-estradiol; 0.05, 0.1 and 0.2 mg/100 g), hydrocortisone (0.5, 1.0 and 3.0 mg/100 g) and dexamethasone (50, 100 and 150 micrograms/100 g). Regucalcin mRNA levels in the kidney cortex were clearly diminished by the administration of aldosterone or estrogen, while hydrocortisone administration had no effect. The administration of dexamethasone (100 micrograms/100 g) caused a remarkable increase of regucalcin mRNA levels in the kidney cortex. The dexamethasone-induced increase in regucalcin mRNA levels was completely blocked by the simultaneous administration of cycloheximide (150 micrograms/100 g), although the drug administration had no effect on the mRNA levels in control rats. Meanwhile, the dexamethasone administration did not cause an appreciable alteration of calcium content in the kidney cortex. The present study demonstrates that, of the various steroid hormones used, dexamethasone uniquely has a stimulatory effect on regucalcin mRNA expression in the kidney cortex of rats. The steroid effect may be mediated through a newly synthesized protein.
Aldosterone↗
The effect of cell K+ on the volume regulation in rat kidney cortex cells.
Incubation of outermost rat kidney cortex slices (rich in proximal tubules) at 0 degrees C in a medium without K+ produces an increase in their cell water, Na+ and Cl- contents and a diminution in their cell K+ content. When these slices are rewarmed at 25 degrees C in a medium without K+, they can regulate their cell volume and their cell Na+ and Cl- contents. When the rewarming period lasts more than 30 min, there is again a cellular swelling, which seems to be correlated with the diminution of the cell K+ concentration. This effect of cellular K+ appears to be related to severe changes in cellular permeability to ions and water. The oxygen consumption and the cell ATP concentrations are similar to those in control conditions. The ouabain-insensitive Na-pump activity is not affected by different concentrations of K+.
Animals↗
Metallothionein and cadmium in human kidney cortex: influence of smoking.
Post-mortem specimens of human kidney cortex of 47 individuals classified according to their smoking habits were analysed for tissue cadmium and cadmium bound to metallothionein. The cadmium content in the kidney cortex of all individuals was 5-99 micrograms/g wet wt. In smokers consuming more than 20 cigarettes/day the mean content of renal cortex cadmium was twice that of non-smokers and amounted to 33.3 +/- 12.5 micrograms/g wet wt. The amount of cadmium bound to metallothionein of all individuals was 0.3-66 micrograms/g wet wt. directly correlating with the cadmium content of the kidney cortex (r = 0.932). More than 50% of renal cortex cadmium was associated with the metallothionein fractions. Due to constant values of zinc and copper in metallothionein the relative amount of zinc and copper to cadmium in metallothionein decreased with increasing tissue cadmium. Together with the elevated binding of cadmium to renal cortex metallothionein, cadmium increasingly was bound to non-metallothionein ligands. These results suggest that, in the renal cortex of smokers with elevated cadmium, a major portion of cadmium is bound to metallothionein. However, it is unclear yet whether the binding of cadmium to metallothionein with subsequent liberation of the metal during degradation of the protein, the impairment of metallothionein functions by the binding of cadmium or the increased binding to non-metallothionein ligands contribute to the toxicity of cadmium in highly exposed individuals.
Adult↗
[An enzymatic method for the isolation of tubules and cells from human kidney cortex].
The isolation of tubules and cells from human kidney cortex was realized by an enzymatic method. Tubules and cells were released from slices of kidney cortex by collagenase. The yield amounted to 80 % of the wet weight of incubated cortex slices. Thus numerous experiments with isolated tubules from one organ could be performed. Glucose production from different substrates was measured in order to test the biochemical integrity of the isolated cells. The highest rates of glucose formation were obtained with fructose as precursor. Glucose production was higher from lactate than from pyruvate. With proline and glutamine as substrates only small amounts of glucose were produced. Glucose formation from 10 mmol/1 pyruvate was linear with time up to 80 minutes. Ado-3':5'-P stimulated glucose formation at 10 mumolar concentration and inhibited gluconeogenesis at 1 mmolar, 0.1 mmolar and 1 mumolar concentrations.
Calcium↗
Calcium-binding protein regucalcin mRNA expression in the kidney cortex is suppressed by saline ingestion in rats.
The effect of adrenalectomy (ADX) or saline ingestion, which is a hypertensive factor, on the expression of calcium-binding protein regucalcin mRNA in the kidney cortex of rats was investigated. The change of regucalcin mRNA levels was analyzed by Northern blotting using rat liver regucalcin complementary DNA (0.9 kb of open-reading frame). Regucalcin mRNA was expressed in the kidney cortex but not the medulla. Rats were adrenalectomized, and 48 h later they were sacrificed. ADX caused a reduction of regucalcin mRNA levels in the kidney cortex, suggesting that adrenal glands participate in the regulation of the mRNA expression. This reduction was not restored by the subcutaneous administration of dexamethasone with an effective dose (1 mg/kg body weight), which can stimulate kidney regucalcin mRNA expression. Regucalcin mRNA levels in the kidney cortex of rats were markedly suppressed by the ingestion of saline for 7 days. The ADX-induced decrease of renal cortex regucalcin mRNA levels was not appreciably restored by saline ingestion. Moreover, regucalcin mRNA levels in the kidney cortex of spontaneous hypertensive rats (SHR) were clearly decreased as compared with that of control (Wistar-Kyoto) rats. Meanwhile, calcium content in the kidney cortex was not significantly decreased by ADX or saline ingestion. The present study suggests that the expression of regucalcin mRNA in the kidney cortex of rats is suppressed by saline administration.
Adrenalectomy↗
Microvascular architecture within the pig kidney cortex.
Corrosion casts of the plastic (Mercox Cl-2B) filled pig kidney cortex vasculature were sliced either parallel or perpendicular to the kidney surface. Scanning electron microscopy photographs were taken of the casts. Montages of the photographs were analyzed using a digitizing tablet and microcomputer-based software. For vessels having diameters larger than 0.05 mm, their sizes, numbers per unit area, and branching patterns were studied with respect to the kidney cortex depth. Vascular branching diameters and angles within the cortex compare favorably with those reported for other major vascular systems. The microvascular dimensions and densities were used to predict the average blood flow velocity within the kidney cortex. It is expected that the results will facilitate a better insight into the contribution of flowing blood to the heat transfer process in perfused tissues.
Animals↗
Catabolism of 6-ketoprostaglandin F1alpha by the rat kidney cortex.
Homogenates of the rat kidney cortex converted 5,8,9,11,12,14,15-hepta-tritiated 6-ketoprostaglandin F 1alpha into one major product identified by gas chromatography-mass spectrometry of the methoxime-methyl ester trimethylsilyl ether derivative as 6,15-diketo-9,11-dihydroxyprost-13-enoic acid. The sequence of derivatisation i.e. methoximation prior to methylation, was crucial as methylation of 15-keto catabolites of the E, F and 6-keto-F series affords degradation products. The corresponding 15-keto-13,14-dihydro catabolite was formed in much smaller quantities. Time course studies indicated that 6-keto-prostaglandin F1alpha was catabolised at a slower rate (about 2-5 fold) than prostaglandin F1alpha. The catabolic activity was blocked by NADH.
Animals↗
Kinetic characterization of phosphofructokinase isolated from rat kidney cortex.
1. Phosphofructokinase from rat kidney cortex has been purified by affinity chromatography to a final specific activity of 15 units per mg of protein, measured at 25 degrees C and pH 8. 2. This lower spec. act., compared with that of the enzyme from other sources, shows the enzyme in proximal tubules to be less active, which would account for the main gluconeogenic role of these nephron sections. 3. The binding of fructose-6-phosphate to the enzyme is co-operative. ATP increases the Hill coefficient and produces a marked allosteric inhibition on the activity. 4. Fructose-2,6-bis-phosphate is a potent activator of the enzyme from this source. It reduces the Hill coefficient of the enzyme and the inhibition constant of ATP. A marked difference between this and the liver enzyme is that the activation is not co-operative.
Adenosine Triphosphate↗
Uptake and acetylation of p-aminohippurate by slices of mouse kidney cortex.
In slices of mouse kidney cortex, p-aminohippurate (PAH) is taken up by the organic anion transport system and then rapidly acetylated to p-acetylaminohippurate acid (PAAH), so that there is little net accumulation of PAH itself. The basic characteristics of this system have been described. Uptake may be measured as the total of PAH and PAAH combined. Both uptake and acetylation are dependent on aerobic metabolism. Succinate strongly inhibits net accumulation but has only a slight effect on the amount acetylated. This is attributed to the stimulation of efflux by succinate. In the mouse, the degree of acetylation as well as uptake varies with sex and strain, as well as with the drug used as substrate. When organic anion transport is employed as a test system for the assay of nephrotoxicity, it is proposed that slices from the mouse possess advantages over some other species in that acetylation and uptake provide dual endpoints.
Acetylation↗