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Biomedical subjects

M Ban

Publications and source records attributed to M Ban.

At least 73 records · Page 4Linked to original sources
PubMed1990

Role of gamma-glutamyltranspeptidase and beta-lyase in the nephrotoxicity of hexachloro-1,3-butadiene and methyl mercury in mice.

Male Swiss OF1 mice received a single oral dose of either 80 mg/kg hexachloro-1,3-butadiene (HCBD) or 80 mg/kg methyl mercury (MeHg). Examination of cryostat kidney sections stained for alkaline phosphatase (APP) revealed damage to about 50% of the proximal tubules after 8 h. Pretreatment with the gamma-glutamyltranspeptidase (gamma-GT) inactivator AT-125 (Acivin, 50 mg/kg i.p., plus 50 mg/kg p.o., reduced the number of damaged tubules by 59 and 58% in mice treated with HCBD and MeHg, respectively. Pretreatment with the two beta-lyase inhibitors, amino-oxyacetic acid (AOAA, 3 x 100 mg/kg p.o.) and DL-propargylglycine (PPG, 300 mg/kg i.p. plus 300 mg/kg p.o.), reduced HCBD nephrotoxicity by 46 and 59%, respectively, but did not protect against MeHg nephrotoxicity. The results support a role for gamma-GT and beta-lyase in the mouse renal toxicity of HCBD and implicate gamma-GT but not beta-lyase in MeHg-induced nephrotoxicity in mice.

Acute Kidney Injury↗
PubMed1989

Acetone compared to other ketones in modifying the hepatotoxicity of inhaled 1,2-dichlorobenzene in rats and mice.

The ability of acetone and 3 other ketone vapours to influence the hepatotoxicity of inhaled 1,2-dichlorobenzene (DCB) was examined in rats and mice. Methylethylketone, methylisobutylketone or cyclohexanone increased liver cytochrome P-450 content and glutathione-S-transferase (GST) activity, but did not affect serum glutamate dehydrogenase (GLDH) activity in rats. Pre-exposure to these ketones enhanced DCB-induced increase in serum GLDH activity (8-63-fold), while the increases in cytochrome P-450 content (33-86%) and GST activity (42-64%) were identical to those resulting from exposure to ketones alone. Each of the 3 levels of exposure to acetone elicited cytochrome P-450 and GST responses comparable with those caused by the other ketones. In spite of that, acetone pre-exposure potentiated (4785 ppm), reduced (10670 ppm) or suppressed (14790 ppm) DCB-induced liver toxicity. In mice, the 3 ketones mentioned above interacted with DCB on centrolobular liver glucose-6-phosphatase (G-6-Pase) while acetone pre-exposure elicited an interactive G-6-Pase response in the mediolobular area alone, suggesting topographic change.

Acetone↗
PubMed1989

A flavonoid inhibitor of 5-lipoxygenase inhibits leukotriene production following ischemia in gerbil brain.

Leukotrienes C4 and D4 are arachidonic acid metabolites that constrict blood vessels and enhance vascular permeability; their biosynthesis is initiated by the reaction of arachidonic acid with 5-lipoxygenase enzyme. After bilateral carotid artery occlusion for 15 minutes and reperfusion of the gerbil brain for 15 minutes, we determined the brain tissue concentrations of leukotrienes C4 and D4 by radioimmunoassay; they had increased from a baseline concentration of less than 1 to a mean +/- SEM concentration of 12.8 +/- 3.9 pmol/g brain. We also studied the effect of a flavonoid 5-lipoxygenase inhibitor on leukotriene production in the reperfused gerbil brain. A water-soluble flavonoid (5-hexyloxy-3',4'-dihydroxy-6,7-dimethoxyflavone 4'-disodium phosphate) was administered intravenously at a dose of 200 mg/kg body wt; 15 minutes later, both carotid arteries were occluded. The enhanced production of leukotrienes C4 and D4 in the reperfused brain was reduced by approximately 80% (from a mean +/- SEM of 12.8 +/- 3.9 to 2.2 +/- 1.3 pmol/g brain) in the presence of the 5-lipoxygenase inhibitor. The flavonoid did not affect the production of prostaglandin D2, the concentration of which also increased in the reperfused ischemic brain.

Animals↗
PubMed1989

Facile synthesis of 8-benzoylthio-2,6-methano-3-benzazocines and 3-benzoylthiomorphinans having small-ring substituents.

Synthesis of 3-cyclopropylmethyl-, 3-cyclobutylmethyl-, and 3-methyl-8-benzoylthio-2,6-methano-3-benzazocines (1j-l) was performed by regio-selective chlorosulfonation of non-narcotic 8-deoxy derivatives (1a-c) followed by reduction and benzoylation. 3-Benzoylthiomorphinans (2h-j) were also obtained by the same method. Compounds having small-ring substituents (1k, 1l, 2i, 2j) were found to be weak but pure mu- and delta-opioid antagonists. The analgetic activity of 1k was almost equal to that of pentazocine.

Analgesics↗
PubMed1989

[The effect of acetate Ringer dextrose (5%) and lactate Ringer dextrose (5%) in surgical patients].

The clinical evaluation of acetate ringer dextrose (AR-D) for hemodynamic status, metabolism of glucose, electrolytes in serum and urine, liver and renal function and acid-base balance were performed in surgical patients compared with lactate ringer solution (LR-D). The 20 patients scheduled for gynecological operations were randomized into 2 groups. After the administration of AR-D or LR-D, we examined their clinical effects. The results suggest that there were no significant differences between AR-D group and LR-D group. We cannot confirm that AR-D is a better solution for surgical patients than LR-D regarding metabolism of lactate, pyruvate and glucose during operations.

Adult↗
PubMed1988

Assessment of the relative hazard involved with airborne irritants with additional hepatotoxic or nephrotoxic properties in mice.

This paper deals with the conversion of the hepatotoxicity of 1,2-dichlorobenzene (DCB), the nephrotoxicity of hexachloro-1,3-butadiene (HCBD) and the respiratory effects of these two toxicants into quantal data. It aims to provide some useful information on the best strategy used for safety evaluation. A reflex bradypnea indicative of irritation of the nasal cavities of mice occurred during a 15-min oronasal exposure to each chemical. A reduction in the development of staining for liver glucose-6-phosphatase (G6-phosphatase) and an increase in the number of damaged tubules in cryostat kidney sections stained for alkaline phosphatase were the measure of toxicity in mice subjected to a whole-body 4-h exposure to DCB and HCBD vapours, respectively. The immediate irritant responses, as well as the delayed liver and kidney responses, were measured at the peak of the chemical's action. These maximum responses were then used to establish the relationships of exposure level effects and also the median active levels of exposure (MALs). The DCB and HCBD MALs responsible for a 50% decrease in the respiratory rate of mice (RD50) were 181 and 211 ppm, respectively. The MAL required for eliciting a 50% decrease in G6-phosphatase staining intensity in DCB-exposed mice was 598 ppm and that associated with 50% of damaged tubules in HCBD-exposed mice was 7.2 ppm. On the basis of these quantitative data, potency ratios indicated that irritation and kidney injury are the primary manifestations of toxicity associated with short-term exposure to DCB and HCBD, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Air Pollutants↗
PubMed1988

Probenecid-induced protection against acute hexachloro-1,3-butadiene and methyl mercury toxicity to the mouse kidney.

Male Swiss OF1 mice received a single oral dose of either 80 mg/kg hexachloro-1,3-butadiene (HCBD) or 40 mg/kg methyl mercury (MeHg). Examination of cryostat kidney sections stained for alkaline phosphatase (APP) revealed damage to about 50% of the proximal tubules after 8 h. Treatment with the organic anion transport inhibitor probenecid (i.p., 3 x 0.75 mmol/kg) did not have any renal effect in normal mice but reduced the number of damaged tubules by 80 and 90% in mice treated with HCBD and MeHg respectively. The results support the conclusion that the toxicity of HCBD and MeHg to the mouse kidney is related to a probenecid-sensitive transport process. It cannot be stated from the present investigation whether the inhibition nephrotoxicity data are related to classic organic anion secretion by the kidney.

Animals↗
PubMed1986

Effects of kallidinogenase on urinary kallikrein excretion and plasma prostanoid concentrations in patients with essential hypertension.

The effects of kallidinogenase on urinary kallikrein excretion, plasma immunoreactive prostanoids and platelet aggregation were investigated in patients with essential hypertension. Urinary kallikrein excretion and plasma 6-keto PGF1 alpha concentration were significantly decreased in these patients. Significant decreases in blood pressure, as well as significant increases of urinary kallikrein excretion and plasma 6-keto PGF1 alpha concentration after kallidinogenase administration were also observed.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

A case of basilar artery occlusion associated with unilateral low origin of the posterior inferior cerebellar artery.

A case of basilar artery occlusion is reported. The patient suddenly developed dizziness and weakness of the right side. Computed tomography scanning showed focal low attenuation in the left quadrangular lobule of the pons. Cerebral angiography demonstrated proximal occlusion of the basilar artery and significant collateral flow in the posterior fossa from the left posterior inferior cerebellar artery (PICA), which arose from the vertebral artery far below the foramen magnum. The literature concerning the origin of the PICA is reviewed.

Arterial Occlusive Diseases↗
PubMed1986

Concentration-related changes in blood and tissue parameters of hepatotoxicity and their interdependence in rats exposed to bromobenzene and 1,2-dichlorobenzene.

Liver damage resulting from 4 h exposure to bromobenzene (BB) (146-957 ppm) and 1,2-dichlorobenzene (DCB) (245-739 ppm) as model toxicants was evaluated in rats. The modifications considered were the increases in serum glutamate dehydrogenase (GLDH) and sorbitol dehydrogenase (SDH) activities and the decreases in centrolobular liver-cell glucose-6-phosphatase (G6-Pase) staining intensity. A linear inverse relationship was established between the logarithmic values of blood enzyme activities and liver G6-Pase staining intensity. In addition, the levels of exposure to each test chemical were found to be linearly related to liver G6-Pase staining intensity and to the logarithmic values of blood enzyme activities.

Animals↗
PubMed1985

Effects of orally administered glandular kallikrein on urinary kallikrein and prostaglandin excretion, plasma immunoreactive prostanoids and platelet aggregation in essential hypertension.

The effects of orally administered glandular kallikrein on urinary kallikrein, aldosterone and prostaglandin E (PGE) excretion, plasma renin activity (PRA), immunoreactive 6-keto PGF1 alpha and thromboxane B2 concentrations and platelet aggregation were studied in 12 patients with essential hypertension (EH). After a 2-week control period, each patient was given orally 450 KU/day of hog glandular kallikrein for 8 weeks. Urinary kallikrein, aldosterone and PGE excretion, and plasma 6-keto PGF1 alpha and thromboxane B2 concentrations were measured by radioimmunoassay. Platelet aggregation was measured by the addition of ADP, collagen or ristocetin with an aggregometer. Urinary kallikrein excretion and plasma 6-keto PGF1 alpha concentration were significantly decreased in patients with EH. There were no significant differences in PRA, urinary aldosterone excretion and plasma thromboxane B2 concentrations between control subjects and patients with EH. There was a significant decrease in blood pressure in patients with EH coinciding with significant increases of urinary kallikrein and PGE excretion and plasma immunoreactive 6-keto PGF1 alpha concentration after administration of glandular kallikrein. There was also a significant inhibition of platelet aggregation induced by collagen in these patients. Thus, a suppression of the kallikrein-kinin-prostaglandin system in patients with EH was found, and a decrease in blood pressure with an increment of urinary kallikrein, PGE excretion, plasma immunoreactive 6-keto PGF1 alpha and inhibition of platelet aggregation in vivo by the administration of glandular kallikrein.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Novel nonnarcotic analgesics with an improved therapeutic ratio. Structure-activity relationships of 8-(methylthio)- and 8-(acylthio)-1,2,3,4,5,6-hexahydro-2,6-methano-3-benzazocines.

Conversion of the 8-phenolic 1,2,3,4,5,6-hexahydro-2,6-methano-3-benzazocines to the corresponding 8-thiophenolic analogues was achieved by three different routes. Diazotization of 8-amino-2,6-methano-3-benzazocine (2) followed by the reaction with CH3SNa afforded 8-(methylthio)-1,2,3,4,5,6-hexahydro-2,6-methano-3-benzazocine (3). Another route using Grewe cyclization was also examined for the synthesis of 3. As the most effective route, Newman-Kwart rearrangement of benzazocines was selected and closely investigated. 8-(N,N-Dimethylthiocarbamoyl)oxy derivatives (6a-e) rearranged to 8-(N,N-dimethylcarbamoyl)thio derivatives (7a-e) in good yields. Reductive cleavage of 7a-e and subsequent methylation or acylations gave the title compounds (3, 8-24). Although analgesic activities of sulfur-containing benzazocines decreased compared to the corresponding hydroxy compounds, the N-methyl derivative (S-metazocine, 8) showed potent analgesic activity.

Acylation↗
PubMed1984

Surface affinity chromatographic separation of blood cells. IV. Relationship between surface hydrophobicity of human peripheral blood cells and their retention behaviour on polyethylene glycol 20M-bonded Sepharose columns.

The partition behaviour of human peripheral blood cells was studied in dextran T40-polyethylene glycol (PEG) 6000 two-phase systems with and without PEG 6000 palmitate as a hydrophobic ligand at pH 7.5 and at the isoelectric points for the four kinds of cells. delta log K, where K is the partition coefficient, is taken as a measure of the hydrophobic interactions between the cell surface and the palmitoyl residue. Its value is dependent on the concentration of palmitate in the partition systems and on the kinds of cells, increasing in the order platelets, granulocytes, lymphocytes and erythrocytes. A linear relationship was found between the retention volumes of these cells, except that of erythrocytes, on a PEG 20M-Sepharose column and their delta log K values determined in the presence or absence of sodium chloride both at the isoelectric points and at pH 7.5.

Adult↗
PubMed1984

Increased plasma cyclic nucleotide concentrations in congestive heart failure.

Plasma concentrations of cyclic nucleotides (adenosine monophosphate (AMP) and guanosine monophosphate (GMP) were measured by an ultrasensitive radioimmunoassay in 138 patients with heart failure due to various causes. Measurements were related to the New York Heart Association classification of symptoms, plasma noradrenaline concentrations, and mean pulmonary artery pressures. Serial concentrations of cyclic AMP and GMP were also measured daily in four patients treated for acute left ventricular failure. Plasma concentrations of cycle AMP were related to the severity of the heart failure, plasma noradrenaline concentrations, and pulmonary artery pressures. Cyclic AMP concentrations fell rapidly after treatment of acute left ventricular failure. Plasma concentrations of cyclic GMP also depended on the severity of heart failure and the pulmonary artery pressure, and decreased sharply with treatment although remaining at a high value. The cyclic GMP concentrations were significantly higher in patients with mitral stenosis than in those with other types of heart failure.

Adult↗
PubMed1984

Oral administration of arginine and citrulline in the treatment of lysinuric protein intolerance.

In two sibling patients with lysinuric protein intolerance (LPI), the therapeutic effect of oral supplement of arginine and citrulline on postprandial hyperammonemia was investigated. Intravenous load of L-alanine (6.6 mmol/kg of body weight), and oral load of L-arginine (0.8 mmol/kg of body weight) or of L-citrulline (1.0 mmol/kg of body weight) during intravenous load of L-alanine were performed to study the preventive effect of arginine or citrulline supplement on hyperammonemia induced by intravenous amino nitrogen load. In the older sibling, the hyperammonemia induced by the intravenous amino nitrogen load was completely prevented by the oral supplement of citrulline, but not completely prevented in the younger sibling. On the other hand, the hyperammonemia was prevented by the oral supplement of arginine only in the younger sibling, but not in the older sibling. In the light of these results, the younger patient received an oral administration of L-arginine and the older patient L-citrulline for the treatment of postprandial hyperammonemia. Two-year observation of each patient revealed that postprandial hyperammonemia and aversion to protein-rich food completely disappeared and that a marked increase of body weight and height was obtained. Furthermore, there was no side effect with these amino acids supplements. The present study suggests that an oral supplement of arginine or citrulline is effective for preventing postprandial hyperammonemia in this disorder.

Administration, Oral↗