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Biomedical subjects

M Nagano

Publications and source records attributed to M Nagano.

At least 307 records · Page 17Linked to original sources
PubMed1983

[An electrophysiological study on peripheral neurotoxicity of 2,3-butanedione, 2,4-pentanedione and 2,5-hexanedione in rats].

A series of studies was made to clarify the relationship of the chemical structures of 2,3-butanedione (2,3-BDione), 2,4-pentanedione (2,4-PDione) and 2,5-hexanedione (2,5-HDione) to neurotoxicity in terms of n-hexane neuropathy and relative neurotoxic potentials, using electrophysiological methods. These compounds are all molecularly symmetrical diketones with 4, 5 and 6 carbons respectively. A 200 mg/kg dose of each compound was administered subcutaneously five days a week to one of three groups of eight rats. This program continued for 40 weeks in the case of 2,3-BDione and 2,4-PDione and for 14 weeks in the case of 2,5-HDione. Electrophysiological studies of the effects of the compounds on the peripheral nerve were performed by measuring maximum motor conduction velocities (MCV) and sensory conduction velocities (SCV) in the tail nerve of the rats. Residual latencies (RL), motor distal latencies (DL), amplitudes of the muscle action potentials (MAP), and amplitudes of the nerve action potentials (NAP) were also estimated. A significant slowing of MCV began to be observed in the 2,5-HDione group at the 6th week and in the 2,4-PDione group at 10th week. At 8th week, a significant decrease in SCV was also observed in these two groups. The degree of reduction in both MCV and SCV was more pronounced in the 2,5-HDione group than in the 2,4-PDione group. In the 2,5-HDione group, the MCV values were more strongly affected than the SCV values. On the other hand, in the 2,4-PDione group the SCV values were slowed more than the MCV values. The amplitudes of MAP and NAP in the 2,5-HDione group decreased significantly at 12th week and at 10th week, respectively. In the 2,4-PDione group, a significant decrease in NAP amplitudes was observed at 16th week and that in MAP amplitudes at 28th week. The 2,3-BDione group showed a decrease in MAP amplitudes at 28th week. The RL and DL were markedly prolonged at an early stage only in the 2,5-HDione group. The gamma-diketone of 6, 7 and 8 normal chains of the aliphatic hydrocarbons has been reported to cause peripheral distal axonopathy with giant axonal degeneration. This disorder is named gamma-diketone neuropathy. In this study, neurotoxic evidence was revealed by 2,4-PDione, which is 5-carbon and symmetrical beta-diketone.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1983

[An experimental study on electrophysiological and histopathological changes in 2,5-hexanedione-intoxicated rats].

An experimental study of neuropathy due to 2,5-hexanedione (2,5-HDione) was performed in rats by using simultaneously both electrophysiological and histopathological methods. Seven rats were given subcutaneously five days a week 200 mg/kg of 2,5-HDione for first 3 weeks and then 300 mg/kg for the next 5 weeks. Nerve conduction velocities in the tail were measured every week and after the respective measurement times one animals was sacrificed for histological study. At the 2nd week of the experiment, 2,5-HDione-treated rat showed a slight morphological changes with swollen axons in the posterior spinal root fiber and tail nerve. A slowing of motor and sensory conduction velocity (MCV and SCV) in the tail was observed in the treated group at the 4th week. Weakness of hindlimbs was apparently seen at the 5th week. At the 6th and 7th week, histological changes including giant axonal swelling, fiber loss, thinning of myelin and demyelination, were prominent in the various regions of the peripheral nervous system. Additionally, degenerative changes of the spermatogenic cells, especially the formation of multinucleated giant spermatids, were markedly observed in the treated rats at the 6th and 7th week.

Animals↗
PubMed1982

Random distribution of the glucose transporter of human erythrocytes in reconstituted liposomes.

The glucose transporter of human erythrocytes was reconstituted with soybean phospholipids by the freeze-thaw/sonication method and the distribution of the transporter molecules in liposomes was studied. The steady state level of glucose transport in reconstituted liposomes showed saturation when increased amounts of the transporter were used for reconstitution. The saturation curve fitted well to a theoretical curve which was derived assuming a Poisson distribution of the transporter. Freeze-fracture electron micrographs showed random distribution of intramembraneous particles on liposomes, irrespective of liposome size or amount of the transporter added. A detailed study showed a parameter of the distribution (the ratio of transporter to liposome) obtained from the transport measurement can be used for the analysis of the distribution of intramembraneous particles, indicating that most of the molecules seen as particles were active in transport.

Blood Glucose↗
PubMed1982

Metabolism of urea and glyoxylate, degradative products of purines in marine animals.

In marine fish and crustacean liver, degradative enzymes able to convert purines to urate have been shown to be located only in the cytosol, and degradative enzymes able to convert urate to urea and glyoxylate, only in the peroxisomes (Noguchi, T., Takada, Y., & Fujiwara, S. (1979) J. Biol. Chem. 254, 5272-5275). The subcellular distribution of these two enzymes involved in further metabolism of urea and glyoxylate in marine animal species was examined by centrifugation in a sucrose density gradient. Urease was located only in the cytosol of crustacean and mollusc liver; no activity was detected with fish liver. In fish, crustacean and mollusc liver, the conversion of glyoxylate to glycine may be mainly catalyzed by alanine : glyoxylate aminotransferase. Hepatic alanine: glyoxylate aminotransferase was located both in the mitochondrial matrix and in the cytosol in each species studied. These findings suggest that peroxisomal urea is transported to the cytosol then degraded to NH3 for the excretion of purine nitrogens, while peroxisomal glyoxylate is transported to the cytosol or mitochondria then converted to glycine for the reutilization of purine carbons.

Animals↗
PubMed1982

Three-dimensional structure of the crystalloid in the microbody of Kloeckera sp.: composite crystal model.

Electron microscopic investigations using the cryosectioning technique, together with electron diffraction, optical diffraction, and computer simulation, were carried out for the determination of the intrinsic structure of the crystalloid in the microbody of Kloeckera sp. The lattice images seen in the cryosections could be changed from one to another by tilting the specimen at an appropriate angle, the images obtained being well consistent with those obtained by computer simulation. The electron diffraction patterns also agreed with those obtained by optical diffraction. The results demonstrated that the crystalloid was composed of two different types of particles, large and small ones, arranged alternately and making up the composite crystal of rock salt structure. Large particles seemed to consist of alcohol oxidase molecules, while the small particles were presumably made up of catalase molecules.

Bacteria↗
PubMed1982

[An experimental study on the neurotoxicity of 2-octanone and 2-hexanol, a metabolite of n-hexane].

An electrophysiological study of the neurotoxicity of 2-octanone (an analogue of methyl n-butyl ketone) and 2-hexanol (a metabolite of n-hexane) was conducted on rats as a part of the study to determine the specific molecular arrangement required for the development of peripheral neuropathy. The compound 2-octanone or 2-hexanol was administered subcutaneously in the daily dose of 400 mg/kg of each compound into the back of seven rats, weighing 290 g, 5 days per week for a period of 21 weeks. Animals treated with 2-octanone for 21 weeks failed to exhibit apparent clinical and neurophysiological evidence except a slight inhibition of weight gain and narcotic effects after treatment with the compound. The same doses of 2-hexanol for 21 weeks caused hypersalivation, gait disturbances, crossing phenomena of hind limbs and a failure of normal growth. Retardation of the conduction velocity in the motor and sensory nerve fibers and the prolonged motor latencies of the tail nerves (distal part) began to appear at the 14th week of the experiment when 9.6 g in the total dose had been given to each animal. These changes were intensified in the subsequent course of the experiment. Our previous experiments and the present results showed that n-hexane barely produced peripheral neuropathy in doses over 10.5 g, and that 2-hexanone (MBK), 2,5-hexanediol or 2,5-hexanedione never failed to produce a neuropathy even in doses less than 9.6 g of each compound. The above results suggest that the neurotoxic potency of 2-hexanol is greater than that of n-hexane but less than that of MBK, 2,5-hexanediol or 2,5-hexanedione.

Animals↗
PubMed1982

Identification and properties of the glucose transporter of human erythrocytes.

Several lines of studies were undertaken to clarify the identity of the glucose transporter of human erythrocytes. Peptide maps of zone 4.5 which is the main component of the purified transporter fraction, were different from those of band 3. Cytochalasin B bound to the purified transporter fraction but not to band 3. Antibody raised against the purified transporter fraction cross-reacted with zone 4.5 and moderately with band 7, but not with other erythrocyte membrane proteins. These results indicate that zone 4.5 is the transporter (or a part of the transporter) and is not a fragment of band 3. With ferritin antibody electron microscopy and freeze-fracture electron microscopy, the glucose transporter were found to evenly distributed in reconstituted liposomes. Further morphological analysis coupled with transport assays showed the distribution of the transporters was random and was satisfactorily fitted to Poisson distribution, indicating reversible association of the transporters does not occur in liposomes and is not necessary for transport activity. This communication summarises our recent studies on identification and properties of the glucose transporter of human erythrocytes. A full account of the studies is published elsewhere (22, 23).

Blood Glucose↗