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E Bogin

Publications and source records attributed to E Bogin.

At least 55 records · Page 3Linked to original sources
PubMed1987

Effect of parathyroid hormone on the fragility and enzyme activities of red blood cells from young and mature rabbits.

The effect of parathyroid hormone on erythrocytes from newborn and adult rabbits was studied in relation to the fragility pattern in hypotonic salt solutions and the activities of Ca- and Mg-dependent ATPases. Median osmotic fragility of red blood cells from newborn rabbits was significantly higher than in red blood cells from mature rabbits. Parathyroid hormone increased the mean osmotic fragility of red blood cells from newborn and adult rabbits, but showed the greater effect on those from newborns. Similarly, the hormone stimulated to a much greater extent the Ca-ATPase, but not the Mg-ATPase in red blood cells from the newborn rabbits, in comparison with red blood cells from adult rabbits. Parathyroid hormone, which is greatly elevated in the blood of patients with chronic renal failure, may be one cause for the anaemia seen in these patients, and its effect, which is mediated by Ca-ATPase activity, is stronger on young red blood cells. Significant morphological changes in the young red blood cells, observed by scanning electron microscopy, were caused by parathyroid hormone.

Aging↗
PubMed1987

Effect of verapamil on plasma parathyroid hormone.

The effects of the Ca antagonist, verapamil, on the behaviour of parathyroid hormone was studied in normal and uraemic male Wistar rats. Parathyroidectomy was by cautery. Acute uraemia was induced by bilateral nephrectomy, and moderate uraemia by s.c. injection of gentamicin (200 mg/kg). Ethylendiamine tetracetic acid (50 mg/kg X d) was injected subcutaneously. Parathyroid hormone was determined by radioimmunoassay. The degree of uraemia was determined from plasma urea levels. Renal failure resulted in a significant increase in plasma parathyroid hormone (mean +/- SEM, ng/l) (84 +/- 6, n = 10, in the control; 277 +/- 39, n = 7, in the moderate uraemics and 667 +/- 128, n = 6, in the acute uraemics). Injection of verapamil significantly increased plasma levels of parathyroid hormone, ranging from 21% in the controls to 62% in the moderate uraemia group. In the acute uraemics, parathyroid hormone levels were very high and verapamil did not cause any further elevation of the hormone in the blood. Parathyroidectomy significantly lowered plasma parathyroid hormone, and verapamil resulted in a mean increase of 29%. EDTA caused an increase of 64%, compared with the control group.

Acute Kidney Injury↗
PubMed1987

Pharmacokinetic changes of several antibiotics in chickens during induced fatty liver.

The concentrations of five antibiotics (erythromycin, lincomycin, penicillin G, streptomycin and oxytetracycline) were determined in chicken serum before and after induced fatty liver. The pharmacokinetic variables were calculated according to the obtained data. The crossover trial design involved 10 chickens for each antibiotic. The fatty liver was produced by oestradiol-dipropionate injections and monitored by serum malic enzyme activity determinations. Protein binding of the respective antibiotics was determined in vitro in the serum obtained from normal and oestrogen-treated birds. Induction of fatty liver caused several changes in the determined variables. The measured peak concentrations were higher for lincomycin and erythromycin and lower for penicillin and oxytetracycline while streptomycin remained unchanged. The peak concentration of streptomycin appeared earlier and the peak of oxytetracycline later than in the normal chickens. The elimination half-lives were shorter for erythromycin, lincomycin and streptomycin and increased for penicillin and oxytetracycline. The area under the concentration curve (AUC) decreased for erythromycin, penicillin and streptomycin, increased for oxytetracycline and remained unchanged for lincomycin. The body clearance (ClB/f) and the apparent specific volume of distribution (Vd(area'/f) were considerably changed in association with fatty liver induction. Since the fraction of the drug absorbed (f) is not known, it can only be speculated that changes in distribution rather than reduced liver function altered the kinetics. The protein binding was decreased for all the antibiotics, but this did not seem to be the reason for changes in kinetics, except perhaps in the case of penicillin.

Animals↗
PubMed1986

Effect of parathyroid hormone and uremia on erythrocyte deformability.

Parathyroid hormone (PTH) caused a significant decrease in human erythrocyte filtration rate (EFR). This effect was Ca2+-dependent and was partially reversed by the Ca2+ blocker verapamil. It was mimicked by the Ca2+ ionophore A-23187. Mg2+ even at high concentrations could not substitute for Ca2+. There was a dose response between the filtration rate and Ca2+ or PTH concentrations. Serum ultrafiltrate of patients with chronic renal failure and secondary hyperparathyroidism caused significant inhibition similar to that seen with PTH extract. Ultrafiltrate from patients with chronic renal failure following parathyroidectomy and from healthy individuals did not cause this phenomenon. Erythroyctes deformability in uremic patients appears to be caused by high PTH levels. Our present findings agree with ones about the toxic effects of PTH on various biological systems.

Calcium↗
PubMed1986

Biochemical changes in liver, kidney and blood associated with common bile duct ligation.

Common bile duct ligation (CBDL) in rats was used to induce liver disease and secondary kidney damage. The biochemical changes in the liver, kidney and plasma were studied at 3, 6, 10 and 21 days post CBDL. The observed alterations climaxed at the 6th day following ligation. Renal, activities of aldolase (ALD), lactic dehydrogenase (LDH), isocitric dehydrogenase (ICDH), sorbitol dehydrogenase (SDH), and alkaline phosphatase (ALP), were lowered in CBDL rats. Further, microsomal Na,K-ATPase and Mg-ATPase and mitochondrial oxidative-phosphorylation were inhibited. In the liver from CBDL rats the activities of aspartate aminotransferase (AST), Mg-ATPase and ALP were elevated, while SDH, ALD, malic dehydrogenase (MDH), LDH, malic enzyme (ME) and Na,K-ATPase were lowered. Plasma enzymes, AST, ALP, MDH, LDH, ALD, acid phosphatase (ACP) and ICDH and the metabolites bile acids, bilirubin, creatinine and urea were elevated. Addition of bile acids or bilirubin at concentrations comparable to those found in the plasma of CBDL rats, to the reaction mixture of the various enzymes strongly inhibited most, particularly mitochondrial oxidative phosphorylation. High concentrations of these substances in the blood may explain the development of renal failure during liver disease and its reversibility when liver function returns to normal.

Animals↗
PubMed1986

Changes in renal enzyme activities following the administration of gentamicin to unilateral nephrectomized rats.

The effects of unilateral nephrectomy and the impact of gentamicin administration on renal tissue enzyme activities in adult Wistar rats were investigated. Gentamicin 200 mg/kg body wt. or an equivalent volume of saline to control rats was administered subcutaneously on three consecutive days, followed by unilateral nephrectomy. Rats were killed on day 3, 7 or 14 following nephrectomy. Alkaline phosphatase, predominantly a proximal tubular brush border enzyme, rose in both the experimental and control groups, however, significantly less in the gentamicin treated rats. Aspartate aminotransferase activity, an enzyme participating in renal glucogenesis, increased transiently in the control but remained unchanged in the experimental group. No difference in glucose-6-phosphate dehydrogenase activity between the two groups was observed, probably reflecting the localization of this enzyme to distal tubular segments, a site unaffected by gentamicin. Significant and similar increases in Mg2+ and Na+ K+ ATPase were observed on day 14 in both groups. The administration of the drug resulted in a marked reduction in oxygen consumption, with a higher oxidation to phosphorylation ratio (P/O). Serum creatinine concentration was significantly higher on days 3 and 7 in the experimental group reverting to control values on the 14th day. Urea concentration increased significantly on days 3 and 7, decreasing on the 14th day to values slightly, but significantly, higher than those of the controls.

Alkaline Phosphatase↗
PubMed1986

Parathyroid hormone effect on the fragility of human young and old red blood cells in uremia.

Parathyroid hormone (PTH) is elevated in patients with chronic renal failure (CRF) and was suggested to be one of the factors responsible for the anemic syndrome of these patients because it raises the osmotic fragility of the red blood cells (RBC). In the present study, the youngest and oldest RBC were separated from circulating erythrocytes by high-speed centrifugation. The age distribution was described, and the effect of PTH on the different age groups was investigated. Median density (MD) and glutamic-oxaloacetic transaminase (GOT) activity were chosen as age markers. MD (1.0985 +/- 0.00087) and GOT activity (12.49 +/- 2.083 IU/g Hb) of the young uremic cells did not differ significantly from the values of young normal cells (1.0987 +/- 0.00046 and 10.36 +/- 1.174 IU/g Hb, respectively). The MD of the oldest cells, however, was lower (1.1048 +/- 0.00054) and GOT was higher (6.60 +/- 1.1019 IU/g Hb) in the uremic than in the control cells (1.1093 +/- 0.00175 and 3.77 +/- 0.233 IU/g Hb, respectively). These results indicate that the life span of RBC in uremics is shorter than normal and that an enrichment of circulating RBC by young cells occurs in uremic patients. The median osmotic fragility (MOF) of the young cells was lower in both uremic (0.376 +/- 0.006) and control patients (0.378 +/- 0.003) than the MOF of old cells (0.402 +/- 0.005 and 0.392 +/- 0.004, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Aspartate Aminotransferases↗
PubMed1986

Biochemical changes in liver and blood during liver fattening in rats.

Excessive fat accumulation in the liver is a common metabolic disorder seen in humans and animals. Fatty liver was induced in the rat by feeding the animals with a sucrose rich diet containing 1% orotic acid for 2-3 weeks. In the sera from fatty liver rats there were significant changes in the level of alanine aminotransferase (+ 68.7%), malic dehydrogenase (+ 77.8%), gamma-glutamyl transpeptidase (- 53.4%) and total lipids (+ 26.6%). There were small to no changes in the levels of aspartate aminotransferase, glucose-6-phosphate dehydrogenase, lactic dehydrogenase, aldolase, malic enzyme, 6-phosphogluconic acid dehydrogenase, alkaline phosphatase and albumin. In fatty liver, significant differences were seen in the levels of glucose 6-phosphate dehydrogenase (+ 235%), malic enzyme (+ 170%), gamma-glutamyl transpeptidase (+ 113%), 6-phosphogluconate dehydrogenase (+ 63%), aspartate aminotransferase (+ 35.6%), malic dehydrogenase (+ 38%), lactic dehydrogenase (+ 37%), and alanine aminotransferase (- 23%). Comparison of the non-fatty part with the fatty part of the fatty liver showed larger changes in the non-fatty part of the liver, suggesting that during the fattening process, there is an induction of enzymes in the liver reaching a peak prior to lipid accumulation, declining thereafter during liver fattening. The increase in NADPH-generating lipogenic enzymes suggests that accumulated fat in the liver is at least partially from de-novo increased synthesis in the liver.

Animals↗
PubMed1985

Sialic acid content of erythrocytes in uremic patients. Correlation with the age distribution of erythrocytes as assessed by glutamic oxaloacetic transaminase determination.

In a previous study we suggested that an enrichment in young red blood cells (RBC) should occur in the erythrocyte population of uremic-anemic patients. This change in RBC age distribution together with the fact that young cells were reported to be richer in sialic acid would provide an explanation for the observed lack of difference in sialic acid content between patients' and controls' whole erythrocyte populations in spite of an increased neuraminidase activity found to be present in patients' serum. To verify this assumption glutamic oxaloacetic transaminase (GOT) activity, which is an erythrocyte age index, and sialic acid were determined in low and high density fractions separated by centrifugation of packed cells representing young and old RBC, respectively, from two groups of 8 individuals with chronic renal failure and two groups of controls. GOT was determined also in whole erythrocyte populations. Mean GOT activity was significantly higher in the young fractions compared to the old of both patients' and control RBC (14.9 vs. 7.8 and 12.4 vs. 7.5 IU/g Hb). Activity of the whole RBC population was significantly higher in uremics as compared to controls (11.7 vs. 5.6 IU/g Hb) which is compatible with a lower median erythrocyte age. Mean sialic acid was higher in the young fractions as compared to the old (42.7 vs. 35.3 nmol/10(9) cells in controls and 48.9 vs. 43.0 nmol/10(9) cells in patients). These differences together with an enrichment in young cells would compensate for the eventual loss of sialic acid in the whole population resulting from an increased neuraminidase-like activity in patients' serum.

Aspartate Aminotransferases↗
PubMed1985

Biochemical change in the liver and kidney of rats following parathyroidectomy.

The effect of hypoparathyroidism and low blood calcium on enzyme levels in rat liver and kidney is shown. Four animal groups were used: parathyroidectomized (PTX), PTX with CaCl2 added in the drinking water, sham-operated controls and sham-operated with CaCl2 added in the drinking water. PTX significantly lowered serum parathyroid hormone (PTH) and calcium. Supplementation of CaCl2 in the drinking water increased serum Ca levels in PTX rats but not in the controls. Significant changes in several liver and kidney enzymes were seen. Most affected were the liver NADP dependent enzymes, glucose-6-phosphate dehydrogenase and malic enzyme. Similar patterns but with relatively smaller changes were seen in the liver enzymes, lactic dehydrogenase, hexokinase, and aspartate transferase. No significant differences between the groups were seen in the levels of malic dehydrogenase, isocitric dehydrogenase, fructose-6-phosphate kinase and cholinesterase. In the kidney, which was less affected than the liver, the only significant difference was seen in the level of malic enzyme. Serum total lipids in the PTX group were significantly lower. All the changes seen were partially reversed by Ca supplementation in the drinking water.

Animals↗
PubMed1983

Effect of parathyroid hormone and uremic sera on the autoagglutination and sedimentation of human red blood cells.

Parathyroid hormone (PTH) caused a dramatic acceleration of erythrocyte sedimentation rate (ESR). This effect was calcium dependent and was partially reversed by verapamil. It was not mimicked by 5 mumol/l calcium ionophore A-23187. Following the removal of PTH from the cell suspension the ESR returned to normal. PTH also caused haemagglutination, the reaction was Ca2+ dependent, pH dependent and was partially reversed by verapamil. High levels of Ca2+ ionophore A-23187 mimicked this phenomenon. Magnesium ions even at concentrations of 5 mmol/l did not replace Ca2+, while Ca2+ at concentrations of 3 mmol/l and above caused haemagglutination. The glycolytic inhibitor NaF at levels of 1 mmol/l did not inhibit haemagglutination. The polyamines pertusin and spermidin, prostaglandins PGE2 and PGF, and the calcium hormone calcitonin, did not reproduce the PTH effect. Dialysate from serum of patients with chronic renal failure and hyperparathyroidism caused haemagglutination, while dialysate from patients with chronic renal failure following parathyroidectomy and normal individuals did not cause this phenomenon. It seems that abnormal erythrocyte behaviour seen in patients with chronic renal failure is caused by PTH which leads to modified Ca2+ metabolism in these cells.

Blood Sedimentation↗
PubMed1983

The effect of jaundiced sera and bile salts on cultured beating rat heart cells.

Jaundiced serum from common bile duct ligated rats, added to cultured heart cells, decreased the beating rate, caused an early cessation of beating and production of higher levels of lactate in the media. Deoxycholate and cholate are the main bile acids in jaundiced serum; deoxycholate caused similar effects, which suggests that it is the toxic substance responsible for heart function alterations seen in patients with severe jaundice.

Animals↗
PubMed1982

Hepatic cirrhosis suggesting aflatoxicosis in a flock of geese.

An outbreak of hepatic cirrhosis in a flock of young geese was investigated. The affected geese were cyanotic with purple beaks, shanks and footwebs. On post mortem examination severe atrophy of the liver was seen and, histologically, extensive areas of necrosis, cirrhosis and bile duct proliferation were prominent. Liver function tests and serum enzyme levels confirmed that the liver damage was extensive. The findings are compared with those found in aflatoxicosis of other avian species.

Animals↗
PubMed1982

Effect of nutrition on fertility and blood composition in the milk cow.

The relationship between nutrition, fertility and blood composition was studied in 400 cows from commercial farms. Fertility evaluated by overall conception rate (OCR) was shown to be significantly related proportion of concentrate and roughage feeds in the diet, and to its content of dry matter, digestible protein, Ca and P. The ratio of serum total lipids to glucose and a newly introduced parameter, delta Pi (a calculated value, obtained by subtracting whole blood levels of Pi from those of the blood serum), showed a highly significant relationship to OCR. No significant relationship was found between OCR and serum, total lipids, cholesterol, urea, Ca, Mg, organic and inorganic phosphate. The values and significance of the 2 blood parameters which showed a relationship to fertility are discussed.

Animals↗
PubMed1982

Effect of parathyroid hormone on osmotic fragility of human erythrocytes.

The survival of erythrocytes (RBC) is shortened in uremia, and it has been shown that calcium influx into RBC evoked crenation and increased their rigidity. The high blood levels of parathyroid hormone (PTH) may augment entry of calcium into RBC and hence affect their integrity. We examined the effect of PTH on osmotic fragility of human RBC and investigated the mechanisms through which PTH interacts with RBC. Both the amino-terminal (1-34) PTH and the intact (1-84) PTH, but not the carboxy-terminal (53-84) PTH, produced significant increases in osmotic fragility. This effect was abolished by prior inactivation of the hormone. There was a dose-response relationship between both moieties of PTH and the increase in osmotic fragility. This action of PTH required calcium, was mimicked by calcium ionophore, and was partially blocked by verapamil. PTH caused significant influx of (45)Ca into RBC, which was not associated with potassium leak. The hormone did not affect water content of RBC. Scanning electron microscopy revealed that the incubation of RBC with PTH was associated with the appearance of membrane filamentous extensions, which anchor RBC together. Inhibition of glycolytic activity of RBC with NaF or inhibition of Na-K-activated ATPase with ouabain did not abolish the effect of PTH on osmotic fragility. PTH did not stimulate RBC Na-K-activated ATPase or Mg-dependent ATPase but caused marked and significant stimulation of Ca-activated ATPase. The basal activity of the RBC adenylate cyclase was low and PTH produced only a modest stimulation of this enzyme. Both cyclic AMP and dibutyryl cyclic AMP had no effect on osmotic fragility. THE DATA INDICATE THAT: (a) the RBC is a target organ for PTH, (b) the hormone increases osmotic fragility of RBC, and (c) this effect of PTH is due to enhanced calcium entry into RBC. We suggest that the increased calcium influx may affect the spectrin-actin of the cytoskeletal network of the RBC and may alter the stability and integrity of the cell membrane. This action of PTH on the RBC could be, at least in part, responsible for the shortened survival of RBC in uremia, and assign a new role for PTH in the pathogenesis of the anemia of uremia.

Adenosine Triphosphatases↗
PubMed1982

Effects of parathyroid hormone on oxidative phosphorylation of heart mitochondria.

In an effort to understand the mechanism of action of parathyroid hormone (PTH) on the myocardium, we examined the effect of PTH on the function of isolated heart mitochondria. The hormone inhibited mitochondrial respiration in the presence of malate or beta-hydroxybutyrate but not succinate as substrates. It also inhibited phosphorylation and uncoupled oxidative phosphorylation. These effects of PTH were dose dependent and occurred only in the presence of calcium. A change in calcium concentration from zero to 2 mM did not affect mitochondrial function. PTH also stimulated mitochondrial ATPase. The inhibitory effect of PTH on mitochondrial respiration and on oxidative phosphorylation would result in decreased ATP synthesis and, hence, reduced availability of ATP. Such a sequence of events may provide an explanation for a potential long-term adverse effect of the hormone on the myocardium.

Animals↗