Biomedical subjects

M Ban

Publications and source records attributed to M Ban.

At least 19 recordsLinked to original sources

PubMed1992

Indirect and lactation-associated changes in renal alkaline phosphatase of newborn rats prenatally exposed to cadmium chloride.

Pregnant Sprague-Dawley rats were intraperitoneally injected with physiological saline solution (vehicle) or cadmium chloride (CdCl2) at 2.5 mg kg-1 body wt. on days 8, 10, 12 and 14 of gestation. Offspring were examined for renal alkaline phosphatase activity (ALP) on postnatal days (PND) 3 and 12, and for kidney metallothionein (MTh) and for liver, kidney and entire gastrointestinal tract 109Cd content at birth and on PND 3 and 12. No effects were observed on neonatal survival or on body, liver and kidney weights of pups up to PND 12. Newborns born and fed by mothers exposed to CdCl2 during pregnancy exhibited a significant decrease in ALP activity on PND 3. Conversely, no significant changes were observed in newborns lactated by surrogate non-treated mothers. Renal MTh increased with age but was not influenced by maternal treatment. Traces of 109Cd were present in the liver at birth (5-7 ng). Thereafter, 109Cd was mainly found in the gastrointestinal tract of newborns lactated by their biological mothers (610-690 ng on PND 12), with a marginal uptake in the liver (10-12 ng on PND 12). 109Cd was not detectable in the kidneys at any age (less than 4 ng). These results show that prenatal exposure to Cd cannot be the sole aetiological agent in the induction of the subtle and transitory changes in renal biochemistry observed in offspring born and fed by female rats intraperitoneally injected with 2.5 mg CdCl2 kg-1 body wt. on days 8, 10, 12 and 14 of gestation. The results also contradict the role of a direct effect on the kidney.

Alkaline Phosphatase↗

PubMed1992

Malignant Langerhans cell tumour.

We report the case of a 49-year-old woman suffering from a malignant neoplasm of Langerhans cells (LC), documented by immunohistochemical and ultrastructural analysis, and review the literature to examine and characterize the clinical and laboratory features, therapy, and prognosis of malignant neoplasms of LC. Langerhans cell histiocytosis is now regarded as a disorder of immune regulation or an inflammatory process, rather than as a malignant neoplasm. Although LC share certain features in common with ordinary histiocytes or interdigitating dendritic cells, they also differ significantly from these cells in other respects. Therefore, we propose designating a malignant neoplasm of LC 'malignant Langerhans cell tumour' and that it should be considered as a separate entity from Langerhans cell histiocytosis or other malignant histiocytoses.

Antigens, CD↗

PubMed1991

Effects of probenecid and acivicin on potassium dichromate-induced acute nephrotoxicity in mice.

Male OF1 mice were injected subcutaneously with 80 mg/kg potassium dichromate (K2Cr2O7). Examination of cryostat kidney sections stained for alkaline phosphatase (APP) revealed damage to about 40-70% of the proximal tubules after 8 h. Pretreatment with the organic anionic transport inhibitor probenecid (i.p., 3 x 0.75 mmol/kg) reduced the number of damaged tubules by 60% in mice treated with potassium dichromate. Pretreatment with the gamma-glutamyltranspeptidase (gamma-GT) inactivator acivicin (AT-125, 50 mg/kg p.o., plus 50 mg/kg i.p.) failed to prevent chromate-induced renal toxicity. These results support the conclusion that a probenecid-sensitive transport process, but not a gamma-GT-catalyzed degradation, is involved in the mouse renal toxicity of potassium dichromate.

Alkaline Phosphatase↗

PubMed1991

Interdependence of polymorphonuclear neutrophils and macrophages stained for N-acetyl-beta-glucosaminidase in lavage effluents from toluene diisocyanate-exposed rat lungs.

Male Sprague-Dawley rats were exposed to toluene diisocyanate (TDI) concentrations between 0.082 and 1.087 ppm for 4 h, and pulmonary lavage was carried out 24 h after initiation of the exposure. Cells recovered from the lavage effluents of TDI-exposed rat lungs were identified and counted, then pulmonary macrophages (PMs) resulting from cytocentrifuged preparations were examined for N-acetyl-beta-glucosaminidase (NAG) cytochemical staining. Exposure to TDI led to a parallel and concentration-dependent increase in the number of polymorphonuclear neutrophils (PMNs) and the proportion of PMs stained for NAG, suggesting that the same primary event initiates the two cell responses.

Acetylglucosaminidase↗

PubMed1991

[Delayed evolution of post-traumatic contralateral extracerebral hematoma after evacuation of initial hematoma].

105 patients over a 5-year period underwent emergency evacuation of traumatic intracranial hematomas. Seven (6.7%) developed delayed contralateral extracerebral hematomas (5 epidural and 2 subdural hematomas). These hematomas were insignificant or not present on initial computed tomography (CT) scan, but repeat CT scan after craniotomy showed sizable hemorrhage. In one patient, neurological deterioration heralded the delayed onset. In one case, intraoperative ultrasound imaging disclosed an epidural hematoma. Ultrasound examination is recommended in cases with a skull fracture contralateral to the initial hemorrhage.

Adolescent↗

PubMed1990

Pregnancy-associated changes in renal toxicity of cadmium-metallothionein: possible role of intracellular metallothionein.

Nulliparous female, 10-day and 20-day pregnant rats were injected intraperitoneally with saline or labelled cadmium-metallothionein (109Cd-MTh) at a single dose of 25 or 250 micrograms Cd as cadmium-metallothionein (Cd-MTh)/kg and sacrificed at 24 h. The renal toxicity was manifested by increased 24-h urinary excretion of beta 2-microglobulin (beta 2-m) and the increased number of damaged convoluted proximal tubules at 24 h. The renal excretion of 109Cd and 109Cd content in the maternal liver and kidney and in the foeto-placental unit were determined. The binding of 109Cd to kidney proteins and the level of intracellular metallothionein (MTh) in livers and kidneys were also determined. It was found that the nephrotoxicity of injected Cd-MTh did not differ in nulliparous and 10-day pregnant rats. This result was consistent with the absence of difference in the renal uptake of 109Cd, its binding to kidney proteins and in the content of endogenous MTh in the kidneys between nulliparous and 10-day pregnant rats. In contrast, 20-day pregnant rats exhibited much more nephrotoxicity than nulliparous rats. The most prominent finding in relation to the extreme sensitivity of 20-day pregnant rats was a lower basal level of intracellular MTh in the kidneys and the accumulation of 109Cd in the high molecular weight proteins in the soluble fraction. It is suggested that the decrease of intracellular MTh in the kidneys of 20-day pregnant rats is the reason for the low protection against the renal toxicity of injected Cd-MTh.

Animals↗

PubMed1990

Decrease in the rat bronchial acetylcholinesterase activity after toluene diisocyanate inhalation.

Acetylcholinesterase (AChE) activity was measured in bronchial tissue homogenate and blood from rats subjected to single and repeated 4-h daily inhalation exposure to toluene diisocyanate (TDI) or control atmospheres. A single 4-h exposure to TDI in the concentration range of 0.7-4.3 ppm did not decrease AChE activity in bronchial tissue but a 4-h exposure to 0.6 ppm TDI, or greater, for two consecutive days did reduce this activity (19% to 33% of the controls). Increasing the level of exposure to TDI for two consecutive days from 0.6 to 4.0 ppm and extending the length of exposure to 1.2 ppm TDI from 2 to 4, 9 or 14 days produced no further decrease in bronchial ACHE activity. Throughout these experiments, blood AChE activity remained unchanged. In rats exposed to 0.3 or 1 ppm TDI for 3 weeks, staining of the bronchial smooth muscle for AChE was reduced (36% of the controls) after exposure to 1 ppm TDI. These results support, for the first time, in vivo and localized anti-AChE activity by TDI.

Acetylcholinesterase↗

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↗