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Biomedical subjects

T Yamano

Publications and source records attributed to T Yamano.

At least 91 records · Page 5Linked to original sources
PubMed1995

Effects of pesticides on isolated rat hepatocytes, mitochondria, and microsomes II.

Twenty-two pesticides were examined in vitro for their effects on hepatocytes, mitochondria, and microsomes isolated from male rats. Twelve pesticides reduced non-protein sulfhydryl (NPSH) content in hepatocytes to less than 80% of control at a concentration of 10(-3) M. Chlorothalonil and ziram were especially effective, reducing NPSH content at 10(-4) M after 90 min incubation. Among those pesticides, only copper terephthalate and chlorothalonil were reactive with glutathione non-enzymatically and enzymatically, respectively. Lipid peroxidation in hepatocytes was stimulated by four pesticides, namely, chlorothalonil, pretilachlor, ethoprofos, and metribuzin at 10(-3)-10(-4) M. Cell viability was considerably decreased following incubation with chlorothalonil, trichlamide, and ziram. Hepatotoxicity of trichlamide was considered to be associated with its direct adverse effects on mitochondrial energy production, since it uncoupled isolated mitochondrial respiration at 10(-6) M and depleted cellular ATP content prior to cell death. Conversely, chlorothalonil- and ziram-induced hepatotoxicity seemed to be related to their depleting effects on cellular sulfhydryls, since addition of the thiol compound dithiothreitol to the hepatocytes incubation mixture protected cells. With respect to isolated mitochondrial respiration, four pesticides inhibited state 3 and/or state 4 respiration rates at 10(-3)-10(-4) M, whereas seven pesticides uncoupled state 4 respiration at 10(-3)-10(-6) M. With respect to isolated microsomal lipid peroxidation, three pesticides were peroxidative at 10(-3)-10(-4) M, whereas three pesticides were antioxidative at 10(-3)-10(-7) M. Only two pesticides, beta-endosulfan and metalaxyl, had essentially no effects on any parameters tested at 10(-3) M.

Animals↗
PubMed1995

[Mechanism on formation of new ipsilateral corticospinal tract following neonatal unilateral cortical ablation in rats].

The corticospinal tract in the rat after neonatal ablation of the unilateral cerebral cortex was studied morphologically using the antegrade horse-radish peroxidase (HRP) tracing method. An aberrant ipsilateral tract was observed 7 days after the operation. Formation of the aberrant neuronal pathway has been confirmed to be contributed mainly by new axons, which ramified at the level of the pyramidal decussation from healthy corticospinal fibers. This ramified axon ran toward the ipsilateral dorsal funiculus. A few fibers also contributed to the aberrant pathway by changing their direction on the way of extension at the level of the pyramidal decussation. These results indicate that the ramification and change of the direction of extending axons play an important role for formation of a new ipsilateral corticospinal tract.

Animals↗
PubMed1994

Pathogenesis of cerebellar deformity in experimental Chiari type I malformation caused by mumps virus.

We sought to elucidate the pathogenesis of Chiari type I malformation using an experimental model of hydrocephalus produced by inoculating hamsters with mumps virus. Dilatation of the lateral ventricules was detected in all brains inoculated at 2, 10, and 25 days of age. The cerebellum in hamsters inoculated at 2 and 10 days of age showed elongation and flattening of the vermis and protrusion or notching of the uvula. All layers, i.e., the molecular, Purkinje cell, and granular layers, and the white matter were preserved, but had become narrow. Purkinje cells remained normal. Hamsters inoculated at 25 days of age did not develop the cerebellar deformity. Mumps virus antigen was detected in all ependymal cells and in some epithelial cells of the choroid plexus in all hamsters that had been inoculated at 2, 10, or 25 days of age. Results suggest that Chiari type I malformation is caused by two main factors occurring simultaneously, i.e., increasing intracranial pressure and rapid histogenesis of the cerebellar cortex.

Animals↗
PubMed1994

Histochemical study of mitochondrial enzymes in cerebellar cortex of macular mutant mouse, a model of Menkes kinky hair disease.

The cerebellar Purkinje cells in the hemizygote of the macular mutant mouse contain numerous abnormal mitochondria which show a marked decrease in cytochrome c oxidase activity. Using histochemical methods we studied the activity of other mitochondrial enzymes, such as NADH diaphorase and succinic dehydrogenase, in the cerebellar cortex of this mutant mouse. Such activities were markedly increased in the Purkinje cells, especially in the soma and stem dendrite, from 10 days after birth in the hemizygote as compared with findings in normal littermates. These results were considered to be due to an increased number of abnormal mitochondria.

Animals↗
PubMed1994

Effects of TRI-n-butyl phosphate on pregnancy in rats.

A teratological study was carried out on the plasticizer tri-n-butyl phosphate (TBP). Pregnant Wistar rats were treated orally on days 7-17 of gestation with TBP at 0, 100, 200, 400 or 800 mg/kg/day in the dose-finding study and 0, 62.5, 125, 250 or 500 mg/kg/day in the subsequent teratological study. Caesarean sections were performed on day 20 of gestation. In the dose-finding study, all of the pregnant rats were killed by the treatment with TBP at 800 mg/kg/day. In the teratological study, salivation and depression of body weight gain, adjusted body weight gain and food consumption were observed at the higher doses of TBP. There were no significant differences between the groups in the incidence of dead or resorbed foetuses, the number of living foetuses and the body weights of living foetuses of both sexes. The incidence of rudimentary lumbar rib increased significantly at 500 mg/kg/day. There were two cases of malformation: a foetus with deformity of fore- and hind-limbs at 400 mg/kg/day in the dose-finding study and conjoined twins exhibiting three fore-limbs and four hind-limbs at 125 mg/kg/day in the teratological study. These malformations were rare in the background data of teratology, and the incidence of foetuses with malformations was not increased significantly. Therefore, TBP was considered not to be teratogenic in this study.

Administration, Oral↗
PubMed1994

Low levels of serum apolipoprotein A I and A II in senile dementia.

We studied the serum lipoprotein and apolipoprotein profiles in 44 patients with sporadic late-onset Alzheimer's dementia and 43 patients with vascular dementia. The levels of high-density lipoprotein (HDL) cholesterol were lower in both patient groups than in a control group. Apolipoprotein A I and A II levels have decreased in both the patient groups, especially in the vascular dementia group. The HDL-cholesterol levels correlated positively with the level of apolipoprotein A I, but not with the level of apolipoprotein A II. The ratios of apolipoprotein A I/A II have increased in both the patient groups. The apolipoprotein A II levels have disproportionally decreased in the patient groups. The serum apolipoprotein A II may involve the pathological process in the patients with senile dementia.

Aged↗
PubMed1994

A new protocol and criteria for quantitative determination of sensitization potencies of chemicals by guinea pig maximization test.

This paper presents precise sensitization test data of 15 chemicals with a wide spectrum of sensitization potencies, and proposes a new protocol and criteria for quantitative evaluation of sensitization potencies of chemicals. The tests were performed according to the design of Magnusson and Kligman, changing the application concentrations for induction as well as for challenge phases. 3-dimensional relationships between mean response (or sensitization rate), induction and challenge concentrations were found in all chemicals tested. The following 2 values are proposed as a quantitative measure of sensitization potency: (a) the minimum induction concentration that induces a positive response; (b) the challenge concentration that induces a mean response approximately equal to 1.0 among the animals applied with the highest concentration for induction. Both values coincided with each other within the range of 1 order of magnitude in every compound except 2. The values varied by 5 orders or more of magnitude among the compounds, showing a wide variation of sensitization potencies among chemicals. A good correlation was found for every chemical between the value of sensitization potency thus obtained and the residual levels in causative products in human cases of allergic contact dermatitis. A new experimental protocol for obtaining values (a) and (b) is proposed.

Allergens↗
PubMed1994

Copper distribution in fetus and placenta of the macular mutant mouse as a model of Menkes kinky hair disease.

Menkes kinky hair disease (MKHD) in humans is caused by a disturbance in copper homeostasis. A mutant mouse shows clinical and biochemical features very close to MKHD. In an attempt to elucidate the defect in copper transport, the copper distribution in various organs of 18-gestational-day-old macular mouse embryos, following administration by a single injection of saline (control) or 50 micrograms of CuCl2 on day 16 of gestation or by two injections on days 15 and 17 of gestation to the dams, was examined both biochemically and histochemically. The copper content in the hemizygous fetus (Ml/y) born to the homozygous mother, who had no copper injection during gestation, was lower in the brain and liver but higher in the placenta than in the respective organs of the normal fetus. When 50 micrograms of CuCl2 was injected into heterozygous dams (Ml/+) on day 16 of gestation, their hemizygous fetuses showed a slight increase in the copper content in the brain and liver, but the amount of copper in these organs was still less than that of the normal fetus. Conversely, the copper content in the placenta of the hemizygous fetus was far higher than that of the normal fetus. In the copper staining of the fetuses harvested from heterozygous dams, some fetuses showed copper deposition in the placenta, but not in the liver. The others showed no copper deposit in both the placenta and liver, thus indicating that the former were hemizygous for the mutation and the latter were normal littermates.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

[Experimental hydrocephalus induced by intraplacental mumps virus inoculation].

Experimental production of congenital hydrocephalus was undertaken by inoculating mumps virus into pregnant hamsters intravenously or intraplacentally. When the mumps virus was inoculated intravenously on the 8th, 10th, 12th, or 14th day of gestation, some fetuses were aborted and those which could come to term did not develop hydrocephalus after birth. Offsprings from the mothers, which had had intraplacental inoculation on the 14th day of gestation, showed ventricular dilatation in about 28%. Histological examination revealed inflammatory infiltration on the surface of ependymal layers, subependymal edema and microglial activation in the underlying ependyma of the aqueduct. These findings were thought to have resulted from ependymitis caused by mumps virus. The transplacental infection of mumps virus is considered to be extremely rare. However, in such conditions as the placental barrier is impaired, mumps virus will possibly pass through the placenta, and will cause hydrocephalus to the infant.

Animals↗
PubMed1994

[A case of clinical Reye syndrome with symmetrical abnormal signal areas in the pons and thalami by MRI].

We report a two-year-old boy with clinical Reye syndrome. Brain CT disclosed symmetrical low-density areas in the pons and thalami, a part of which was recognized as being of high-intensity on both T1 and T2 weighted MRI. These lesions were suspected of being caused by vascular involvement, since the methemoglobin induced by bleeding may have contributed to the high-intensity regions. The lesions gradually disappeared within four months after the onset, and clinical symptoms also improved markedly without serious neurologic impairment. This case was characterized by the marked improvement in neurological and radiological findings in spite of the serious neurological involvement at onset.

Child, Preschool↗
PubMed1993

Effects of pesticides on isolated rat hepatocytes, mitochondria, and microsomes.

Twenty-seven pesticides, with which people are concerned, especially as residues in food, were examined in vitro for their effects on hepatocytes, mitochondria, and microsomes isolated from male rats. Nineteen pesticides returned non-protein sulfhydryl (NPSH) contents in hepatocytes to less than 80% of control at concentrations from 10(-3) to 10(-5) M after 90 min incubation. Among them, only dichlofluanid was reactive with glutathione non-enzymatically. Lipid peroxidation in hepatocytes was stimulated by five pesticides at 10(-3) M, with edifenphos being the most potent peroxidant. Cell viability was considerably decreased by incubation with chlorobenzilate, edifenphos, dichlofluanid, and chinomethionat at 10(-3) M, and in these cases, depletion of cellular adenosine 5'-triphosphate (ATP) contents proceeded to cell death. With respect to isolated mitochondrial respiration, six pesticides inhibited state 3 and/or state 4 respiration rates at concentrations from 10(-3) to 10(-5) M, whereas three pesticides uncoupled state 4 respiration at 10(-3) M. With respect to isolated microsomal lipid peroxidation, seven pesticides, five of which were organophosphorus compounds, were peroxidative at concentrations from 10(-3) to 10(-5) M, whereas seven pesticides were antioxidative at concentrations from 10(-3) to 10(-7) M. Only three pesticides, aldicarb, maleic hydrazide, and chlormequat chloride had no effect on any parameters tested at 10(-3) M. Pesticides that affected isolated mitochondria or microsomes did not necessarily have any effect on isolated hepatocytes.

Animals↗
PubMed1993

Neuropathological study on cerebellum of macular mutant mouse heterozygote.

The hemizygote of the macular mutant mouse is clinically, biochemically and neuropathologically similar to a patient with Menkes kinky hair disease. The heterozygote of this mutant mouse was biochemically and neuropathologically examined. The copper content in the brain decreased in comparison with that in the normal littermate, although it was more than that in the hemizygote. In the Golgi study, abnormal Purkinje cells with somal sprouts, thick stem dendrites and dendritic focal swellings, which were seen in the hemizygote, were not observed in the heterozygote. Ultrastructurally, abnormal mitochondria were seen in the Purkinje cells in the anterior and middle cerebellar lobe of the heterozygote. Histochemically, cytochrome c oxidase activity decreased, especially at the anterior lobe in the cerebellar cortex of the heterozygote. This activity, as indicated by staining intensity, was in between that in the normal littermate and that in the hemizygote. The heterozygote did not show a mosaic pattern in the distribution of these neuropathological changes, although this mutant mouse shows x-linked recessive inheritance. Thus, our results lead to the conclusion that the neuropathological changes observed in this mutant mouse do not result directly from an abnormal gene in the Purkinje cell, but from the secondary effects of subsequent to presumptive copper deficiency.

Animals↗
PubMed1993

Histochemical and ultrastructural pathology of skeletal muscle in a patient with abetalipoproteinemia.

Pathological examination was carried out of the skeletal muscle of an 8-year-old boy with abetalipoproteinemia. The patient complained of diarrhea, and showed a deficiency of betalipoprotein, decreased fat-soluble vitamins, acanthocytosis and a mild increase in serum creatine kinase. The prominent histochemical finding was punctate deposits of acid phosphatase activity in most fibers. Ultrastructural lesions revealed a number of giant lysosomes. Although these pathological findings seemed to be related to vitamin E deficiency, other pathological findings such as concentric laminated bodies or filamentous bodies were also observed. The clinical course and the changes in the pathological findings in our patient after long-term vitamin E therapy need to be observed.

Abetalipoproteinemia↗
PubMed1993

Early ependymal changes in experimental hydrocephalus after mumps virus inoculation in hamsters.

To elucidate the pathogenesis of early ventricular dilatation in hydrocephalus, we examined early morphological changes in ependymal layers at the lateral ventricles in suckling hamsters without aqueductal stenosis 5 days after the intracerebral inoculation of mumps virus. Mumps virus antigen was detectable in all ependymal cells. The ependymal cilia had almost disappeared and only the microvilli remained. A number of supraependymal cells were also observed on the surface of the lateral ventricles. Transmission electron microscopy revealed intracytoplasmic viral-like inclusions in the infected ependymal cells. These results suggest that functional and morphological disturbances in infected ependymal cells may cause early ventricular dilatation before aqueductal stenosis occurs.

Animals↗
PubMed1993

Effects of diethylene glycol monomethyl ether on pregnancy and postnatal development in rats.

The effects of oral treatment of Wistar rats with diethylene glycol monomethyl ether (diEGME) were examined. In a preliminary dose-finding study with non-pregnant rats, diEGME treatment at doses up to 4,000 mg/kg/day on 11 consecutive days decreased relative weights of thymus and pituitary gland, white and red blood cell counts, hemoglobin concentrations and hematocrit levels. In pregnant rats, treatment at doses of > 3,000 mg/kg/day (over gestation days 7-17) caused total resorption of all litters. In teratology and postnatal studies, pregnant rats were treated with diEGME at doses of 0, 200, 600, and 1,800 mg/kg/day from day 7 through 17 of gestation. At 200 mg/kg, there were no adverse effects on either dams, fetuses, or neonates. At 600 mg/kg, dams were not affected, but fetal body weights were decreased, and fetal thymus and ossification were adversely affected. At 1,800 mg/kg, maternal thymus weights and food consumption were decreased, and visceral malformations of the cardiovascular system were seen in 28.0% of the fetuses. Only 6.3% of the pups delivered by dams treated with 1,800 mg/kg of diEGME survived for 4 days after birth. Thus, diEGME was teratogenic in Wistar rats, but the spectrum differed from that in Sprague-Dawley rats. In addition to teratogenicity, diEGME had significant adverse effects on postnatal development. The most sensitive organ to diEGME was the thymus in both dams and fetuses.

Abnormalities, Drug-Induced↗
PubMed1993

Characterization of the electron acceptors of old yellow enzyme: mechanistic approach to the mode of one electron transfer from the enzyme to menadione or dyestuffs.

Molecular oxygen or cytochrome c has been described as the electron acceptor of the reaction of old yellow enzyme with NADPH. In this study, menadione was found to be a sensitive electron acceptor of the reaction under aerobic as well as anaerobic conditions. The Km value of menadione for old yellow enzyme is as low as 2-3 x 10(-7) M in the presence or absence of superoxide dismutase. The rate enhancement of the cytochrome c reduction of old yellow enzyme with NADPH was about eight times in the presence of menadione. The rate increment was slightly higher under aerobic than anaerobic conditions. The rate enhancement by menadione enabled sensitive determination of the enzyme activity in the assay system, which contained NADPH, cytochrome c, menadione, and old yellow enzyme. In the reaction course, the semiquinone species of menadione was trapped by the reaction with t-butyl-alpha-phenylnitrone. The radical adduct was detected on EPR. The dyestuff, 2,6-dichlorophenolindophenol, was found to be reduced ineffectively even in the presence of menadione; moreover, it was inhibitory in the NADPH consumption reaction. Methylene blue or Lauth's violet, known to be capable of semiquinone formation, also behaved, like menadione, as a mediator of electron transport to cytochrome c. On the basis of the experimental results, the occurrence of the one electron transfer of the old yellow enzyme reaction was emphasized.

2,6-Dichloroindophenol↗