Biomedical subjects

M Ban

Publications and source records attributed to M Ban.

117 records · Page 7Linked to original sources

PubMedDate not supplied

Postnatal hepatic and renal consequences of in utero exposure to halothane or its oxidative metabolite trifluoroacetic acid in the rat.

In utero exposure of rats to low levels of the anaesthetic halothane has been reported to produce ultrastructural changes in the liver and kidney at birth. The current study examined the postnatal functional capacities of the liver and the kidney following prenatal exposure to halothane. Halothane or its oxidative metabolite trifluoroacetic acid (TFAA) were given to Sprague-Dawley rats on gestational days 10-20. Halothane was administered by inhalation at concentration of 50 or 500 ppm 6 h-1 day-1, and TFAA was administered by gavage at doses of 75 or 150 mg kg-1 day-1. The exposed offsprings were examined on postnatal days 3, 12 or 49 for hepatic and renal biochemistry and/or function through measurements of several serum and urinary parameters. Neither halothane nor TFAA treatments had statistically significant effect on litter size, neonatal survival or postnatal growth. Both prenatal halothane and TFAA exposure produced changes in liver biochemistry of newborns, as indicated by significant increases in the serum activities of glutamate dehydrogenase and aspartate aminotransferase. In addition, TFAA caused a functional deficit of the proximal tubule in newborns, as evidenced by the significant increase in the urinary excretion of beta 2-microglobulin. However, these hepatic and renal alterations were restricted to the early postnatal period and were no longer observed by postnatal day 49. It is concluded that prenatal exposure to relatively low levels of halothane can cause slight and transient changes in the neonatal rat liver.

Age Factors↗

PubMedDate not supplied

Role of SAM-dependent thiol methylation in the renal toxicity of several solvents in mice.

The role of S-adenosylmethionine (SAM)-dependent thiol methylation in the nephrotoxicity of seven industrial solvents was studied in mice. The seven following solvents were utilized: bromobenzene (BB), styrene (STY), tetrachloroethylene (TTCE), trichloroethylene (TCE), 1,1-dichloroethylene (DCE), 1,2-dichloroethane (DCA) and hexachlorobutadiene (HCB). The experimental model comprised mice pretreated with periodate oxidized adenosine (ADOX) (100 micromol kg(-1) i.p.) 30 min before injection of solvents. In the first 4 h after ADOX treatment, the SAM levels were about fourfold higher than controls for the liver and kidney. The S-adenosylhomocysteine (SAH) levels were increased by factors of 11 and 14 and the SAM/SAH ratios were decreased by factors of 3 and 10 for the liver and kidney, respectively. These results show that ADOX treatment probably induces an inhibition of methyltransferase SAM-dependent in the liver and kidney and thus decreases the methylation capabilities. A single oral administration of BB (500 or 800 mg kg(-1)), TTCE (3500 or 4000 mg kg(-1)), TCE (3000 or 3500 mg kg(-1)) or STY (400 or 600 mg kg(-1)) did not induce renal toxicity, evaluated by the percentage of damaged tubules compared to controls. On the other hand, the three solvents DCE, HCB and DCA were nephrotoxic and the percentage of damaged tubules observed for each solvent was significantly different from the value of <1.8% for controls: 19% and 40% for DCE (130 and 200 mg kg(-1)), 50% and 46% for HCB (80 and 100 mg kg(-1)) and 5.1% and 7.6% for DCA (1000 and 1500 mg kg(-1)). The ADOX treatment in the mice did not modify the renal toxicity of the seven solvents. Thus, their renal toxicity, when it existed, was probably independent of the SAM-dependent thiolmethyltransferase activity in the mice. The results of this study are discussed from two viewpoints. The first concerns the general considerations on inhibition of thiol methyltransferase activities in mice and the second is related to the different solvents that are evoked individually.

Adenosine↗

PubMedDate not supplied

Immune complex transfer two-site chemiluminescent immunoassay for serum growth hormone in alevin chum salmon.

An immune complex transfer two-site chemiluminescent immunoassay (CLIA) for salmon growth hormone (GH) was developed to measure serum GH in alevin chum salmon (Oncorhynchus keta) using a chemiluminescent acridinium ester as a label. The immune complex transfer method dramatically reduced non-specifically bound of acridinium ester labelled antibody without a decrease in the specific binding. Consequently, we could detect lower levels of GH than achieved previously in a two-site CLIA for salmon GH. The detection limit of the assay was 7.8 fg/ml and the standard curve was linear up to 250 fg/ml. Coefficients of variation were 2.2-7.7% within-assay and 5.3-91% between-assay. We have developed a highly sensitive and reproducible GH method and applied it to measurement of GH in alevin chum salmon.

Acridines↗

PubMedDate not supplied

Partial contribution of biliary metabolites to nephrotoxicity, renal content and excretion of [14C]hexachloro-1,3-butadiene in rats.

Male Sprague Dawley rats with cannulated bile duct (BDC rats) received 100 or 200 mg kg-1 labelled hexachloro-1,3-butadiene ([14C]HCBD) by gavage 1 h (BDC1 rats) or 24 h (BDC24 rats) after surgical cannula implantation. Twenty-four hours after treatment with HCBD, rats were examined histochemically and biochemically for kidney damage. Urine, faeces, liver and kidney radioactivities were also measured in 24-h samples. Results were compared with those obtained from non-cannulated (NC) rats. Bile-duct cannulation did not completely protect against HCBD-induced kidney damage. The 24-h [14C] urinary excretion and tissue content was 30-50% lower in BDC rats compared to NC rats and correlated well with the toxicity findings. BDC1 rats appeared to be much more resistant to HCBD treatment than BDC24 rats. Since faecal [14C] radioactivity extractable by diethyl ether at neutral pH in BDC1 rats was twice that measured in BDC24 rats, the greater resistance was attributed to a higher deficiency in the gastrointestinal absorption of unchanged HCBD. The present results reveal that the biliary metabolites of HCBD are not solely responsible for kidney toxicity as previously assumed. They suggest a sinusoidal efflux of the HCBD conjugates from the liver.

Animals↗

PubMedDate not supplied

Urinary thiodiglycolic acid and thioether excretion in male rats dosed with 1,2-dichloroethane.

1,2-dichloroethane (DCE) is extensively metabolized and partially excreted in urine as thioether compounds, which include thiodiglycolic acid (TDGA). In this study, we have compared the urinary excretion of TDGA and thioethers in the rat after administration of increasing doses of DCE. Male Sprague Dawley rats were given a single oral dose of labelled [14C]DCE (0.125 to 8.08 mmol kg-1 body wt.) and 24-h urine samples were collected. The TDGA and thioethers were determined in urine by a gas chromatography method and by the thioether assay after alkaline hydrolysis, respectively. The percentage of the administered radioactivity that was excreted in urine decreased with increasing dose of DCE and ranged between 63 and 7.4%. The amount of TDGA increased proportionally to the DCE dose up to 1.01 mmol DCE kg-1 body wt. and corresponded to 0.22 mmol TDGA mmol-1 DCE. Up to 0.25 mmol DCE kg-1 body wt., the amount of thioethers recovered in urine was not significantly different as compared to the vehicle control group (11.8 +/- 0.6 mumol SH equiv. kg-1 body wt., n = 10). From the 0.25-4.04 mmol DCE kg-1 body wt. dose, the amount of thioethers increased linearly with the dose of DCE and corresponded to 0.028 mmol SH equiv. mmol-1 DCE. The ratio between urinary thioethers and TDGA increased with the DCE dose and reached 0.17 +/- 0.01 (n = 5) at a dose of 8.08 mmol DCE kg-1 body wt. Moreover, TDGA contents determined in urine by gas chromatography before and after alkaline hydrolysis were not significantly different.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Lipofibromatous hamartoma of the median nerve associated with macrodactyly and port-wine stains.

Lipofibromatous hamartoma of the nerve is a very uncommon congenital tumor. An association between this condition and vascular malformations is not well known. We present an 11-year-old girl with a lipofibromatous hamartoma of the right median nerve with macrodactyly. She had small red macules on her right neck, chest, and arm, which were diagnosed clinically as port-wine stains. The specimens of the enlarged nerves showed fibrous and fatty growth surrounding the nerve bundles and proliferation of the small veins. We suggest that this disorder can be accompanied by a vascular malformation.

Child↗

PubMedDate not supplied

Myocardial concentration of norepinephrine and cyclic AMP in ventricular fibrillation during acute myocardial ischemia.

To clarify the relationship between the concentrations of norepinephrine (NE) and cyclic AMP (c-AMP) in the myocardium and the incidence of ventricular fibrillation (VF), we studied 48 dogs in which VF was induced by the ligation of the left anterior descending coronary artery. The animals were divided into two groups of equal size: The first received no drugs, the second received d,l-propranolol (0.5 mg/kg) 15 min before coronary ligation. Myocardial samples were taken at regular intervals from normal and ischemic areas to determine NE and c-AMP concentrations. In the untreated group, no significant change in the concentrations of NE and c-AMP was observed in 12 dogs that did not develop VF. In the other 12 dogs that developed VF, there was a significant increase in c-AMP in the ischemic area immediately after the onset of the dysrhythmia. A significant increase in NE concentration both in normal and ischemic myocardium was observed in only 8 of these latter 12 dogs. Premedication with propranolol significantly reduced the incidence of VF, but it still occurred in 5 out of 24 dogs. Increase in c-AMP without an increase in NE in ischemic area was observed in these five dogs. These results suggest that c-AMP may play a role in the development of VF during acute ischemia.

Animals↗

PubMedDate not supplied

Hair follicle nevi and accessory tragi: variable quantity of adipose tissue in connective tissue framework.

Controversy exists about the histologic differences between hair follicle nevi and accessory tragi. We examined 10 congenital lesions histologically, possible diagnoses of which were hair follicle nevi or accessory tragi. Two specimens out of the 10 had tiny, mature hair follicles surrounded by thick fibrous root sheaths, a few fat cells, and no cartilage. The subcutaneous fat cells of their bases were segmented by a connective tissue framework. They had histologic features of hair follicle nevi. One specimen had cartilage and abundant fat cells with a connective tissue framework in the nodule, as well as a conglomeration of numerous well-differentiated hair follicles. It possessed both elements of a hair follicle nevus and an accessory tragus. Seven specimens had abundant subcutaneous fat and showed a prominent connective tissue framework. These were typical accessory tragi. The present study suggests that the number of fat cells in the nodule or papule differs between these two conditions. All the lesions studied revealed a connective tissue framework in the subcutaneous fat. Histologic features of both hair follicle nevi and accessory tragi can coexist in a single lesion. Hair follicle nevi may represent incomplete accessory tragi with scant fat cells.

Adipose Tissue↗

PubMedDate not supplied

Dopamine-beta-hydroxylase activity after acute myocardial infarction.

After acute myocardial infarction, serial serum dopamine-beta-hydroxylase (DBH) activity was elevated in both high and low DBH subgroups. The observed increase in DBH activity on the first, second, and third days after acute myocardial infarction suggests an augmentation in sympathetic nervous system activity after acute myocardial infarction.

Acute Disease↗