Biomedical subjects

F Akahori

Publications and source records attributed to F Akahori.

5 recordsLinked to original sources

PubMed1992

An analytical study of antibacterial residues in meat: the simultaneous determination of 23 antibiotics and 13 drugs using gas chromatography.

Simultaneous determination of 7 penicillins, 3 tetracyclines, 5 aminoglycoside antibiotics, 5 macrolide antibiotics, 2 polyether antibiotics, chloramphenicol and 13 drugs was evaluated. The 36 agents in meat were extracted with 10% trichloroacetic acid. The extracted solutions were adsorbed on an Amberlite XAD-2 resin column and an activated carbon resin column and then eluted with methanol and 0.01N HCl-methanol, respectively. The eluted solutions were concentrated to dryness and trimethylsilylated with pyridine, N, 0-bis (trimethylsilyl) acetamide, N-trimethylsilylimidazole and trimethylchlorosilane. They were then measured by gas chromatography with a flame-ionization detector. The recovery for almost all of the 36 compounds from the original meat specimens was more than 82%. The limits of detection for most of the 36 agents using this method were equivalent to the original individual methods of analysis.

Aminoglycosides↗

PubMed1992

Acute toxicological studies on paraquat: pathological findings in beagle dogs following single subcutaneous injections.

Sixteen beagles were allocated into 4 groups, each group consisting of 2 males and 2 females, which were injected sc with 1,3,5 or 7 mg paraquat/kg. The beagles were observed for 2 w after the administration. At the end of the observation period all the dying and surviving dogs were studied pathologically. The LD50 was calculated as 1.8 (1.0-6.1) in males and 3.5 (2.4-10.1) mg/kg in females. Clinical laboratory tests showed increases in segmented neutrophils and monocytes, decreases in lymphocytes, slight decreases in chloride, moderate increases in BUN, GOT, GPT and phospholipids, slight increases in uric acid, total protein, creatine, total cholesterol and total bilirubin, and prolonged prothrombin times. Marked edema, congestion and hemorrhage of lungs, as well as slight congestion in various organs, were observed grossly. In histopathological examination, marked pulmonary hemorrhage and congestion, fibroblast-like cells in alveolar septa, breakdown of alveolar walls, thickening of alveolar walls and pleura, mild congestion and degeneration of the liver, and mild degeneration of renal tubules were observed. The cause of death was respiratory distress and renal failure. The surviving animals had mild atelectasis of the lungs. Electromicroscopic examination on the surviving animals revealed the appearance of spindle-shaped cells, proliferation of type II alveolar cells and fibroblasts, mitosis of fibroblasts, and abundant collagen fiber in the lung, calcium deposition, stratification and thickening of basement membranes, and localized necrotic epithelial cells in the proximal tubules of kidneys, and stratification of intramitochondrial cristae of the liver. Pulmonary fibrosis in the switchover stage was present with participation from type II alveolar cells, fibroblasts and myofibroblasts.

Animals↗

PubMed1992

Subacute toxicity of paraquat in beagle dogs: clinicopathology and pathologic examinations.

Beagle dogs were allocated to 4 groups, each consisting of 3 males and 3 females, which received 0.055, 0.165 or 0.495 mg paraquat (PQ)/kg/day sc for 4 w to investigate subacute toxicity. Recovery 4 and 8 w postadministration was studied. In the early stage there was vomiting, decreased activity and undernourishment. Induration and ulcers at the injection sites were seen. The group receiving 0.495 mg PQ/kg had reduced food ingestion and occasional decreases in water consumption until the end of the 4-w injection period. Three animals in the 0.495 mg PQ/kg group were sacrificed in the moribund stage with marked decreases in body weight. Ophthalmologic examination at 4 w of recovery detected hemorrhage around the nasalis vein of the left fundus in 1 animal that received 0.495 mg PQ/kg. No abnormal changes in electrocardiography (ECG) were noted throughout the experimental period. Slightly increased urinary protein, reticulocyte counts, and fibrinogen were observed in a few animals in each group. A few animals that received 0.165 or 0.495 mg PQ/kg had increased phospholipid, blood urea nitrogen, and creatine phosphokinase. The lungs of the moribundly sacrificed animals had moderate atelectasis, localized atelectasis, moderate thickening of alveolar wall and pleura, proliferation of fibroblast-like cells, and abundant fibers in interstitium and alveoli. In the liver there was slight hemorrhage along the gallbladder. On electron microscopy of the lung, proliferation of fibroblasts, myofibroblasts and type II alveolar cells, and some mast cells were observed in thickened alveolar walls. Abundant collagen fibers, destroyed cell debris and mitotic figures of spindle-shaped fibroblasts were also observed in the dilated interstitium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1991

Effects of azamethiphos, an organophosphorus insecticide, on serum cholinesterase activity and isoenzymes in the rat.

The inhibitory effect of azamethiphos (Az), an organophosphorus insecticide, was detected in both the serum cholinesterase (ChE) activity and the ChE isoenzyme concentration in male Wistar rats. In our highest Az dosage group (270 mg/kg), following a single po administration, the serum ChE activity was significantly inhibited at 6 and 24 h post-Az administration. Five days after Az treatment, the ChE activity was still inhibited, but the observed difference was not statistically significant. The ChE activity increased to levels comparable to the control group by day 10. For the other Az-dosed groups, the ChE activities were inhibited only 6 h following administration. The serum ChE isoenzymes for all Az-dosed and control groups had 6 bands, indicating that Az did not effect the number of isoenzyme bands, indicating that Az did not effect the number of isoenzyme bands. However, Az had a significant effect on the ratios of the concentrations of these isoenzyme bands. The ratio of the main ChE isoenzyme bands (bands 5 and 6) was band 6 greater than band 5 for the young control group. As our control group aged, this ratio was reversed, with band 5 greater than band 6. For the highest Az dosage group (270 mg/kg), the ChE isoenzyme band ratio was band 5 greater than band 6 6 h after Az dosing. This proportion of band 6 decreased in parallel with an increase in band 5 during our 30-d experimental period. A correlation between the total ChE activity and ChE isoenzyme band 6 was found.

Animals↗

PubMed1979

Effects of dietary cadmium on rhesus monkeys.

Ten male rhesus monkeys, each weighing 3.5 kg, were divided into four groups of 3, 3, 2, and 2, and were fed daily with 100 g pelleted food containing 300, 30, 3, and 0 ppm cadmium, respectively. Urine samples were collected every 2 weeks and blood samples every 4 weeks. One monkey each of the 300 and 30 ppm groups was autopsied for pathological examination and tissue cadmium determination at the week 24 of the experiment; the remaining 8 animals were killed after 55 weeks. The lowest exposed group (3 ppm) did not show any specific biological response to cadmium over a period of 55 weeks. In the 30 ppm group, no significant changes were observed for up to 24 weeks, although cadmium concentration in the renal cortex and urine at 24 weeks were 300 mug/g wet weight and 18 mug/l., respectively. Plasma urea nitrogen and urine protein (quantitative determination) increased after 30 and 36 weeks. At 55 weeks of the experiment, qualitative tests were negative for low molecular weight proteinuria and glycosuria, and the results remained normal for renal and liver function tests and blood analysis, although cadmium concentrations in the renal cortex of two monkeys were 460 and 730 mug/g wet weight and those in the liver were 110 and 160 mug/g wet weight, respectively. In the highest exposure group (300 ppm), urine cadmium increased to 250 mug/l. by 11 weeks, and urine retinol-binding protein, plasma GOT, GPT, and LDH increased after 12 weeks. Proteinuria (quantitative determination), glycosuria, aminoaciduria (panaminoaciduria), and erythrocytopenia were observed after 16 weeks, when urine cadmium was 500-900 mug/l. Hypohemoglobinopathy and proteinuria (qualitative determination) were observed after 20 and 24 weeks, while cadmium concentrations in the renal cortex and the liver were 760 and 430 mug/g wet weight at 24 weeks, respectively. Slightly depressed tubular reabsorption of phosphate, increased urine beta(2)-microglobulin, increased plasma urea nitrogen, and increased plasma alpha(2)-globulin fraction (electrophoresis) were observed between 28 and 30 weeks of the experiment. Creatinine clearance and plasma cholinesterase decreased after 47 and 54 weeks, respectively. Cadmium concentrations in the renal cortex and the liver of two monkeys at 55 weeks were 350 and 580 mug/g wet weight and 410 and 630 mug/g wet weight, respectively. Pathological examinations revealed denaturation, destruction, and regeneration of the epithelial cells in renal proximal tubules, but no pathological changes in osseous tissues. Critical cadmium concentration in the renal cortex was estimated to be 380 mug/g wet weight for low molecular weight proteinuria and 470 mug/g wet weight for proteinuria, glycosuria, and aminoaciduria. Critical concentration in the liver was also estimated to be 210 mug/g wet weight. The apparent biological half-time of cadmium in monkeys at autopsied stage was calculated to be 0.66, 6.4, 5.2, and 22.4 years for the 300, 30, 3, and 0 ppm groups, respectively.

Animals↗