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PubMed2006

Suramin-induced reciprocal changes in glucose and lactate synthesis in renal tubules contribute to its hyperglycaemic action.

Suramin is the drug of choice for the treatment of African trypanosomiasis and onchocerciasis. It is also tested for its potential use as an anticancer agent and chemosensitizer. As suramin has been reported to induce hyperglycaemia, its effect on glucose formation has been studied in isolated rabbit hepatocytes and kidney-cortex tubules. In contrast to hepatocytes, in kidney-cortex tubules suramin augments glucose production and decreases lactate formation. Suramin-induced changes in intracellular gluconeogenic/glycolytic intermediates indicate a decrease in flux through pyruvate-phosphoenolpyruvate step. Moreover, this compound diminishes pyruvate kinase activity in kidney-cortex cytosolic fraction, while fructose-1,6-bisphosphate ameliorates its inhibitory action. As (i) kidneys are important contributors to the whole body glucose homeostasis and (ii) suramin is known to accumulate in kidney, suramin-induced stimulation of glucose formation in renal tubules might be responsible for hyperglycaemia observed in patients undergoing suramin treatment.

Animals↗
PubMed2005

Renal and hepatic accumulation of cadmium and lead in the expression of CYP4F2 and CYP2E1.

The present study examined accumulation of the metal toxins cadmium (Cd) and lead (Pb) in relation to the abundance of cytochrome P450 4F2 (CYP4F2), CYP2E1 and concentrations of zinc and copper in liver and kidney samples using immunoblotting coupled with metal analysis. The post mortem liver and kidney cortex samples were from 23 males and 8 females aged 3-89 years. All were Caucasians who had not been exposed to metals in the workplace. Average kidney cortex Cd load of 17.4 microg/g w.w. was 17 times greater than average liver Cd load (1.1 microg/g w.w.). In contrast, average kidney cortex Pb load of 0.09 microg/g w.w. was two times lower than liver Pb load of 0.19 microg/g w.w. Average Zn and Cu concentrations in the kidney cortex samples were 67% and 33% lower than those in the liver. Liver and kidney Cd loads, but not liver or kidney Pb loads, correlated positively with donors' age. After controlling for liver Cd load, an inverse correlation was seen between Zn and age (partial r=-0.39, P=0.02), suggesting reduction in liver Zn levels in old age. Liver CYP2E1 protein abundance correlated with age-adjusted Cd load (partial r=0.37, P=0.02) whereas kidney CYP4F2 protein abundance showed a positive correlation with age-adjusted Cd loads (partial r=0.40, P=0.02). These findings suggest that Cd may be an inducer of renal CYP4F2 and hepatic CYP2E1 and that increased renal CYP4F2 expression may implicate in Cd-linked renal tubular dysfunction and high blood pressure, involving CYP4F2-dependent arachidonic acid metabolism.

Adolescent↗
PubMed1985

Pathophysiology of the kidney in rats with Heymann nephritis.

Alterations in kidney function were assessed early in the course of Heymann nephritis that was induced in rats by immunization with Fx1A, an extract prepared from rat kidney cortex. Whole kidney and single nephron function were evaluated by clearance and micropuncture techniques. Kidney function was studied in stage 1 of Heymann nephritis, before the onset of proteinuria, and in stage 2, when antibodies are deposited along the brush border of proximal tubules. Although overall kidney function was similar in rats in stage 1 and normal controls, glucose reabsorption was somewhat depressed in the first part of the proximal convoluted tubule in stage 1. Both whole kidney and single nephron glomerular filtration rates were depressed in stage 2. Proteinuria in stage 2 was characterized by an increased albumin sieving coefficient, which resulted in an elevated excretion of albumin. Furthermore, several proximal tubule functions (glucose and fluid reabsorption and PAH extraction) were substantially depressed in stage 2. These findings demonstrate that immunological injury to the proximal tubules in stage 2 of Heymann nephritis produces a significant impairment of proximal function.

Albumins↗
PubMed1992

Energy metabolism and renal ischemia.

In renal preservation, the longer the organ is cold stored the greater the damage to the organ. The mechanism of hypothermic-induced kidney injury is not known. In this study the effects of long-term preservation (up to 120 h) of the dog kidney on mitochondrial functions in an homogenate of kidney cortex tissue was investigated. Kidneys were exposed to either warm ischemia (0 to 90 min) cold ischemia (0, 72, 96, and 120 h). The mitochondrial oxygen uptake was measured in an homogenate. In both warm and cold ischemia there were changes in the mitochondrial utilization of oxygen. The changes were characterized as a decrease in uncoupler stimulated oxygen uptake by up to 40%, an increase in oligomycin-sensitive respiration by up to about 150%, and a decrease in the respiratory control ratio (uncoupler control ratio) from about 3 to 1. These changes in mitochondrial utilization of oxygen were partially reversed by including albumin in the respiration medium. Albumin binds free fatty acids and these may originate, during ischemia, from the action of phospholipases during ischemia. The changes in mitochondrial oxygen uptake may result from both the loss of membrane-bound phospholipids and the accumulation of free fatty acids. The changes in mitochondrial activity between 72 h (viable kidneys on transplantation) and 96 to 120 h preservation (nonviable kidneys) were not significant. Furthermore, reperfusion of kidneys preserved for 72 to 120 h resulted in a restoration of mitochondrial oxygen uptake to near normal (control) values. Thus, it does not appear that the limitation of successful long-term renal preservation is due to mitochondrial injury caused by cold ischemia.

Animals↗
PubMed1989

Lipid peroxidation: a possible mechanism of trichloroethylene-induced nephrotoxicity.

The purpose of this study was to investigate whether lipid peroxidation plays a role in (TCE) trichloroethylene-induced nephrotoxicity in mice at different oxygen concentrations. Male NMRI mice (25-30 g) were treated i.p. with TCE in a dosage of 125-1000 mg/kg in sesame oil. To determine the TCE-induced depletion of reduced glutathione (GSH) in the kidney cortex and liver tissue, mice were given 1000 mg/kg TCE i.p., then killed between 0 and 6 h after TCE administration and GSH was measured was non-protein sulfhydryls. In another series of experiments, mice were administered 125 to 1000 mg/kg TCE i.p. with or without a 2 h i.p. pretreatment with 1500 mg/kg L-buthionine-S-R-sulfoximine (BSO). Mice were then exposed to a 10, 15, 20 or 100% oxygen atmosphere for 3 h and lipid peroxidation in vivo was measured as exhalation of ethane. Subsequently, mice were killed and malondialdehyde (MDA) generation was measured in the liver and kidney cortex. Ethane evolution was estimated by gas chromatography and MDA was determined as thiobarbituric acid reactive substances. In a further series of experiments mice were treated in the same manner as for ethane and MDA determination and the changes in blood urea nitrogen (BUN) and accumulation of the organic ion p-aminohippurate (PAH) were determined. PAH accumulation by renal cortical slices were measured as the slice to medium (S/M) ratio. Six hours after administration of 1000 mg/kg TCE to mice, GSH was significantly depleted to about 60% of control in the kidney cortex but not in the liver. Three hours after TCE administration, MDA content in the kidney cortex and ethane exhalation increased in a dose-dependent manner only under a 10% oxygen atmosphere. Under the same experimental conditions, MDA content remained unchanged in the liver. BSO depletion of GSH prior TCE administration induced an increase of the MDA content in the kidney cortex and an increase of the ethane exhalation in vivo. At 10% oxygen concentration, TCE induced a dose-dependent increase in BUN and a dose-dependent decrease of PAH accumulation by the renal cortical slices. Thus, the results of the present study suggest that, under hypoxic conditions, lipid peroxidation plays a role in TCE nephrotoxicity.

Animals↗
PubMed1994

Cadmium concentration in the renal cortex of kidney tumor patients and controls.

In this pilot study the concentration of cadmium was determined quantitatively in samples of renal cortex of 22 kidney cancer patients and 19 controls. Data on the three main sources of exposure to cadmium-diet, cigarette smoking and occupation-were obtained through interviews. No significant difference in Cd concentration between the tumor samples and the controls could be found. The mean Cd concentration was 50.9 +/- 25 mg/kg dry weight for cancer patients and 55.2 +/- 50 mg/kg for controls. Further, it was established that the age-dependent relationship for cadmium in the cortex was not valid for smokers.

Adult↗
PubMed1986

Cholecystokinin-destroying activities of canine tissue homogenates.

We have studied the capacity of different canine tissue homogenates to destroy cholecystokinin in vitro. Tissues from the kidney cortex, lung, pancreas, and small bowel contained significant cholecystokinin-destroying activity. Only small amounts of activity were found in the liver, and no activity was detected in the kidney medulla, the gastric antrum, gallbladder, spleen, or in serum or plasma. The kidney cortex was the richest source of activity. The cholecystokinin-destroying enzyme isolated from the kidney cortex was heat-labile, non-dialyzable, and trypsin-resistant, with an optimum pH between 7 and 7.4. The enzyme was inhibited by chelating agents and by phenylalanine amide, although it was little affected by phenylalanine itself or proteinase inhibitors. The enzyme required divalent cation cofactors for its activity. After inhibition by EDTA, the enzyme could be reactivated completely with Mn2+, but not with Ca2+ or Mg2+ alone. The cholecystokinin-destroying enzyme was bound strongly to membranes, and during differental centrifugation, was sedimented with mitochondrial fractions of kidney cortex. The supernatant fraction of the solubilized enzyme obtained at 105,000 X g had a molecular weight of about 480,000 dalton. Since the enzyme could be inhibited by phenylalanine-amide, it would appear to act at the C-terminal end of the cholecystokinin molecule.

Animals↗
PubMed1984

Immunological and physicochemical evidence for tissue specific prolactin receptors in the rabbit.

Late pregnant and midlactating rabbit tissues (adrenal gland, kidney cortex, liver, mammary gland, and ovary) were examined for evidence of tissue specific differences in PRL receptors by several criteria. These included analysis of association constants, gel filtration, analytical isoelectric focusing, and reactivity with specific anti-PRL receptor antibodies in both the direct competition and immunoprecipitation assays, using membrane bound and Triton X-100 solubilized receptors. Association constants of membrane bound PRL receptors were not significantly different (adrenal, 1.50 +/- 0.26 X 10(10) M-1; kidney cortex, 0.90 +/- 0.22 X 10(10) M-1; liver, 1.31 +/- 0.50 X 10(10) M-1; mammary, 0.95 +/- 0.36 X 10(10) M-1) except the ovarian receptor, which had a significantly higher affinity (2.05 +/- 0.04 X 10(10) M-1) than other tissue receptors. This difference did not result from a difference in tracer degradation. Higher affinity for the ovarian receptor may be a consequence of phospholipid modulation of receptor affinity, since Triton X-100 solubilization abolished this difference in affinity (ovary, 3.63 +/- 0.15 X 10(10) M-1; adrenal, 3.48 +/- 0.44 X 10(10) M-1; mammary, 3.61 +/- 0.41 X 10(10) M-1). However, both the solubilized kidney cortex receptor (2.68 +/- 0.52 X 10(10) M-1) and the solubilized liver receptor (2.40 +/- 0.38 X 10(10) M-1) were significantly different from PRL receptors in the other tissues, implying a possible structural distinction. In addition, clear differences in isoelectric point and immunoreactivity were evident between the kidney cortex receptor and PRL receptors in other tissues. Immunologic evidence of differences between mammary gland, adrenal, ovary, and liver PRL receptors was also obtained, although the degree of difference in the liver receptor was obscured by binding of 125I-ovine PRL to the GH receptor. No differences were seen in elution position of solubilized receptors by gel filtration on Sepharose CL6B. These differences support the notion of structurally distinct PRL isoreceptors in different tissues, although it is also possible that they result from differing proportions of two receptor forms (e.g. plasma membrane and golgi complex forms). It is suggested that the kidney cortex receptor is derived from a more primitive form of the PRL receptor concerned with the regulation of electrolyte balance, whereas PRL receptors in other tissues arose at later times to subserve other specialized functions.

Adrenal Glands↗
PubMed1990

Stimulation of mitochondrial pyruvate transport in rat renal cortex by phenylephrine.

Phenylephrine effect on liver and kidney cortex mitochondrial pyruvate concentration was investigated. While in liver the alpha 1-adrenergic agent produced a decrease in pyruvate content, a significant increase was observed in kidney, even in the presence of 0.5 mM alpha-cyano-4-hydroxy-cinnamate. These changes were not observed when pyruvate was formed by intramitochondrial transamination of alanine, suggesting a role for the pyruvate transport across mitochondrial membranes in the regulation of mitochondrial pyruvate metabolism in kidney cortex. This was corroborated measuring the phenylephrine effect on pyruvate carboxylation.

Alanine↗
PubMed1980

Postnatal changes of some enzymatic activities of energy supplying metabolism in the cortex, inner and outer medulla of the rat kidney.

1. In rat kidney cortex, outer and inner medulla the development of activities of seven enzymes was investigated during postnatal ontogeny (10, 20, 30, 60 and 90 days of age). The enzymes were selected in such a manner, as to characterize most of the main metabolic pathways of energy supplying metabolism: hexokinase (glucose phosphorylation, HK), glycerol-3-phosphate dehydrogenase (glycerolphosphate metabolism or shunt, GPDH), triose phosphate dehydrogenase (glycolytic carbohydrate breakdown, TPDH), lactate dehydrogenase (lactate metabolism, LDH), citrate synthase (tricarboxylic acid cycle, aerobic metabolism, CS), malate NAD dehydrogenase (tricarboxylic acid cycle, intra-extra mitochondrial hydrogen transport, MDH) and 3-hydroxyacyl-CoA-dehydrogenase (fatty acid catabolism, HOADH). 2. The renal cortex already differs metabolically from the medullar structures on the 10th day of life. It displays a high activity of aerobic breakdown of both fatty acids and carbohydrates. Its metabolic capacity further increases up to the 30th day of life. 3. The outer medullar structure is not grossly different from the inner medulla on the 10th day of life. Further it differentiates into a highly aerobic tissue mainly able to utilize carbohydrates. It can, however, to some extent, also utilize fatty acids aerobically and produce lactate from carbohydrates anaerobically. 4. The inner medullar structure is best equipped to utilize carbohydrates by anaerobic glycolysis, forming lactate. This feature is already pronounced on the 10th day of life, its capacity increases to some extent during postnatal development, being highest between the 10th and the 60th day of life.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMedDate not supplied

Cadmium levels in feed components and kidneys of growing/finishing pigs.

Cadmium (Cd) concentrations in pig feeds (one control feed and one feed with reduced nitrogen content), straw, water, and pig kidney cortex were determined in 2 breeds of growing/finishing pigs (n = 96). The total Cd intake from feed was calculated. Feed mixtures and components, straw and kidney cortex samples, and certified reference samples were microwave-digested and analyzed by atomic absorption spectrometry with graphite furnace technique. Total Cd concentration in the control feed was 37.1 micrograms/kg wet weight (w.wt). The highest Cd levels were found in nonlocally produced feed components: vitamin-mineral mixture, lime, dicalcium phosphate, soybean meal, and rapeseed meal. These components contributed 70% of the Cd content in the feed. The main component, barley, which was locally produced, contributed 30% of the total Cd content in feed. The feed with reduced nitrogen content contained less soybean and rapeseed meal and a lower Cd level than the control feed. The Cd levels in kidney cortex varied from 38.0 to 105 micrograms/kg w.wt, with a mean level of 70.9 micrograms/kg. The levels differed between breeds and feeds, but not between gender. There was a significant correlation between Cd level in kidney cortex and age at slaughter, with an increase of 2.8 micrograms/kg w.wt in the kidney for each additional week of survival. The contribution of Cd from nonlocally produced feed components could have environmental effects through application of farmyard manure to local soils.

Animal Feed↗
PubMed1988

Selenium, zinc, copper and cadmium concentration in livers and kidneys of people exposed to environmental cadmium.

Selenium (Se), Cadmium (Cd), Zinc (Zn) and Copper (Cu) concentrations have been determined in the kidney cortex, medulla and liver of 21 Cd-exposed and 15 nonexposed autopsied subjects. In the kidney cortex, all four metals were significantly lower in the Cd-exposed subjects than in the nonexposed ones. In the liver Se levels were almost the same in both groups. Significant correlation coefficients between Se and the three metals were found in the kidney cortex of all the subjects. In the liver significant correlation coefficients were only seen between Se and Cu in the Cd-exposed subjects. These results indicated that the distribution of Se in humans chronically exposed to environmental Cd is different from that in humans exposed to environmental organic mercury.

Aged↗
PubMed1987

Tissue-specific differential induction of ornithine aminotransferase by estradiol in rats of various ages.

The level and induction of ornithine aminotransferase of the liver and kidney cortex were determined at different phases of the life span of female rats. The level of this enzyme in the liver did not change significantly till adulthood and decreased thereafter. However, there was no significant differences in the level of this enzyme in the kidney cortex of the rat throughout its life span. Further, the level of this enzyme in the kidney cortex was more than 2.5-fold higher than that of the liver in all the age groups. Ovariectomy decreased, and 17-beta-estradiol increased significantly, the activity of the kidney cortex enzyme in rats except for the old ones. The effects of both these treatments were highest in the young-adult (13-weeks) rats. In contrast, the liver enzyme was irresponsive towards both these treatments.

Age Factors↗
PubMed1984

Functional and morphologic studies of the adrenal cortex and kidney in ovine toxaemia of pregnancy.

Functional and morphologic studies of the adrenal cortex and kidney have been carried out in pregnant sheep with spontaneous or dietary restriction-induced ovine toxaemia. It was found that proteinuria was an inconstant feature and no animal showed glomerular lesions analogous to those found in human preeclampsia; thus ovine toxaemia cannot be regarded as a precise experimental model for human toxaemia of pregnancy. The elevation of blood cortisol levels and the morphologic appearance of the adrenal zona fasciculata found in such animals suggest an adrenal response comparable to that caused by adrenocorticotrophic hormone. In addition, animals with severe disease showed evidence of stimulation of the renin-angiotensin-aldosterone system as reflected by elevated blood renin and aldosterone concentrations and raised renal juxtaglomerular indices. Ultrastructural changes in the adrenal zona glomerulosa and renal juxtaglomerular myoepithelioid cells in toxaemic animals resembled those described in non-pregnant sodium-depleted sheep. The finding of juxtaglomerular peripolar cell mitoses and granule exocytosis, the latter only being previously observed in sodium depleted sheep, together with the ultrastructural changes in the adrenal zona glomerulosa and juxtaglomerular myoepithelioid cells, suggest that sodium depletion may play a role in this disease.

Adrenal Cortex↗
PubMed1987

Metallothionein, cadmium, copper and zinc levels of human and rat tissues.

Metallothionein (MT), zinc (Zn), copper (Cu) and cadmium (Cd) were determined in 10 tissues (brain, heart, kidney cortex, liver, lung, muscle, pancreas, small intestine, spleen and stomach) from human autopsies (10 male individuals, mean age 43 +/- 9 years, all smokers) and Wistar rats. The mean tissue concentrations of MT in the human samples varied between 3.8 and 495 micrograms/g wet weight in spleen and kidney cortex, respectively. In most tissues human MT levels were high as compared to rats; particularly in liver and kidney cortex human MT levels exceeded those of rats about 25- and 10-fold, respectively. Positive linear relationships were observed between Zn or Cu and MT in human liver and between Cd and MT in human kidney cortex.

Adult↗
PubMed2003

Thromboxane synthase and TP receptor mRNA in rat kidney and brain: effects of salt intake and ANG II.

A TP receptor (TP-R) mimetic causes salt-sensitive hypertension and renal afferent arteriolar vasoconstriction. TP-Rs mediate effects of ANG II on renal vascular resistance and drinking. Therefore, we investigated the hypothesis that thromboxane A(2) synthase (TxA(2)-S) and/or TP-R expression is regulated by salt and/or ANG II. Rats (n = 6) received high-salt (HS) or low-salt (LS) diets. Additional HS-diet rats received ANG II while other HS- and LS-diet rats received the AT(1) receptor (AT(1)-R) antagonist losartan. Excretion of thromboxane B(2) by conscious rats was increased with the HS diet compared with the LS diet (126 +/- 10 vs. 48 +/- 5 pmol/24 h, respectively; P < 0.01). The mRNA abundance for TP-Rs (relative to beta-actin) in the kidney cortex was enhanced 30% by the HS diet (P < 0.001) and was reduced 50% by the addition of ANG II (P < 0.001). However, during losartan administration, the effects of salt were reversed; mRNA more than doubled during the LS diet (P < 0.001). Similarly, the mRNA abundance for TP-Rs in the brain stem was reduced by 50% with the addition of ANG II (P < 0.001) and during losartan administration was almost doubled by the LS diet (P < 0.001). The mRNA abundance for TxA(2)-S in the kidney cortex also was increased many times with the HS diet (P < 0.001). In contrast, the mRNA for TxA(2)-S in the brain was unaffected by salt. ANG II did not affect TxA(2)-S at either site. During losartan administration, TxA(2)-S increased modestly in the brain stem with the LS diet. mRNA abundance for TP-Rs in the kidney cortex and brain stem is suppressed by ANG II acting on AT(1)-Rs. In the absence of AT(1)-Rs, expression of TP-Rs at both sites is enhanced by LS intake. In contrast, ANG II does not affect the mRNA abundance for TxA(2)-S. Expression of TxA(2)-S is enhanced by HS intake in the kidney cortex but by LS intake in the brain stem only during losartan administration. Thus TP-Rs are strongly dependent on ANG II acting on AT(1)-Rs, whereas TxA(2)-S is regulated differentially in the kidney cortex and brain stem by salt intake.

Angiotensin II↗
PubMed1988

Immunohistochemistry of cytochrome P-450 21-hydroxylase: microscopic examination of the enzyme in the bovine adrenal cortex and kidney.

Cytochrome P-450 specific for steroid 21-hydroxylase (P-450C21) localized in bovine adrenal cortex and kidney was immunocytochemically observed by the peroxidase-antiperoxidase method using a specific antibody. P-450C21 was present in all three zones of the adrenal cortex. Immunoreactivity for P-450C21 was intense in the zona glomerulosa and inner reticularis and faint in the area between the zona glomerulosa and outer fasciculata, probably representing the zona intermedia. The positive stain was only observed in parenchymal cells. The immunoreactivity varied within each zone, especially in the zona reticularis. In the kidney, immunoreactivity for P-450C21 was exclusively localized in the distal and cortical and medullary collecting tubules. This corresponds to the site of mineralocorticoid action in the kidney. No immunoreactivity was observed in the liver and aorta.

Adrenal Cortex↗
PubMed1995

Membrane fatty acid composition of tissues is related to body mass of mammals.

Phospholipids were extracted from tissues (heart, skeletal muscle, kidney cortex, liver and brain) of mammals representing a 9,000-fold range in body mass (mouse, rat, rabbit, sheep and cattle) and their fatty acid composition was determined. In heart, skeletal muscle and kidney cortex, there were significant allometric decreases in the Unsaturation Index (UI; average number of double bonds per 100 fatty acid molecules) with increasing body mass. There were significant inverse allometric relationships between body mass and the proportion of docosahexaenoic acid (22:6 omega 3) in heart and skeletal muscle. In heart, skeletal muscle and kidney cortex, larger mammals also had shorter fatty acid chains in their phospholipids and a higher proportion of monounsaturates. In liver, smaller mammals had a higher UI than larger mammals (except the rabbit, which had the lowest UI and very low proportions of omega 3 fatty acids). The brain of all mammals maintained a high UI with similar levels of polyunsaturated fatty acids, especially 22:6 omega 3. Our results suggest that in heart, skeletal muscle and kidney cortex the activity of the elongases and desaturases are reduced in large mammals compared to small mammals. The allometric trends in membrane composition may be involved in modifying membrane permeability. It is proposed that the elevated degree of polyunsaturation in the membranes of several tissues from small mammals is related to their higher metabolic activity.

Animals↗