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H Torii

Publications and source records attributed to H Torii.

At least 73 records · Page 4Linked to original sources
PubMed1985

Metabolism of idebenone (CV-2619), a new cerebral metabolism improving agent: isolation and identification of metabolites in the rat and dog.

Metabolic studies of idebenone (CV-2619), a new cerebral metabolism improving agent, in the rat and dog by thin-layer chromatography, gas-liquid chromatography-mass spectrometry and fast atom bombardment-mass spectrometry led to characterization of the following metabolites: the parent compound, 6-(9-carboxynonyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (QS-10), 6-(7-carboxyheptyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (QS-8), 6-(5-carboxypentyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (QS-6), 6-(3-carboxypropyl)-2,3-dimethoxy-5-methyl-1,4-benzoquinone (QS-4), 1- or 4-phenyl sulfate of the hydroquinone derivatives of CV-2619 and QS-4, and 1- and 4-phenyl glucuronides of the hydroquinone derivative of QS-10. These results indicated that CV-2619 was metabolized by oxidation of the side chain followed by beta-oxidation to form successively QS-10, QS-8, QS-6 and QS-4, and reduction of the quinone ring and subsequent conjugation yielding the sulfates and glucuronides of the hydroquinone derivatives of CV-2619, QS-10, QS-8, QS-6 and QS-4.

Animals↗
PubMed1985

Disposition of idebenone (CV-2619), a new cerebral metabolism improving agent, in rats and dogs.

After oral administration of 14C-labeled idebenone (14C-CV-2619) to rats, the plasma 14C level reached a plateau at 15 min, which persisted till 8 h and then decreased with a half-life of 4.5 h. In dogs, after oral dosing, the plasma 14C peaked at 15 min, followed by biophysical decline with half-lives of 2.2 and 15.4 h. The plasma of both animals contained mostly metabolites, with a small amount of unchanged CV-2619, which was greater than 90% protein-bound. In rats given 14C-CV-2619 orally or intravenously, 14C was distributed widely in tissues, with relatively high concns. in the gut, liver and kidney. CV-2619 readily entered the rat brain to undergo subcellular distribution with a significant amount localized in mitochondria. The concn. of 14C in rat fetus was low, as was that in the milk. Oral 14C-CV-2619 was eliminated by rats and dogs mostly as metabolites within 48 h. In rats, more was excreted in urine than in feces, whereas in dogs excretion by these two routes was almost equal. Enterohepatic cycling of biliary 14C occurred in rats. Repeated oral ingestions of 14C-CV-2619 to rats resulted in no accumulation of 14C. The metabolites found in rats and dogs were QS-10, QS-8, QS-6 and QS-4 formed by oxidative shortening of the side chain of CV-2619, and desmethylated CV-2619 and QS-4. Glucuronides and sulfates of the dihydro (quinol) derivatives of the above metabolites were also detected. Dihydro QS-4 sulfate was the major metabolite in plasma and urine of both animals, while dihydro QS-10 glucuronide was predominant in rat bile.

Animals↗
PubMed1985

Metabolism of ipriflavone (TC-80) in rats.

Metabolic studies of ipriflavone (TC-80) in rats by gas-liquid chromatography-mass spectrometry led to the characterization of the following metabolites: the parent compound, 7-hydroxy-3-phenyl-4H-1-benzopyran-4-one, 7-hydroxy-3-(4-hydroxyphenyl)-4H-1-benzopyran-4-one, 3-(4-hydroxyphenyl)-7-isopropoxy-4H-1-benzopyran-4-one, 2-(3-phenyl-4-oxo-4H-1-benzopyran-7-yl)oxypropionic acid, 2-[3-(4-hydroxyphenyl)-4-oxo-4H-1-benzopyran-7-yl]oxypropionic acid and 2-[3-(3-hydroxyphenyl)-4-oxo-4H-1-benzopyran-7-yl]oxypropionic acid. From the metabolites identified, TC-80 was shown to be metabolized primarily by oxidation. In vitro study using tissue slices of rats indicated that the above metabolic changes occurred exclusively in the liver. It was also demonstrated that the compound did not undergo metabolic conversion by gut flora of rats.

Animals↗
PubMed1985

Disposition of ipriflavone (TC-80) in rats and dogs.

Oral 14C-ipriflavone was absorbed by rats to give a maximum plasma 14C level at 1.5 h and a half-life of 5.8 h. In dogs, after po dosing, the plasma 14C peaked at 0.5 h, followed by gradual decline. The plasma of both animals contained mostly metabolites, with small amounts of unchanged ipriflavone. In rats, 14C was distributed widely in tissues, with relatively high concns. in the liver, kidney and gut. Distribution in rat thigh bone of unmetabolized ipriflavone was also demonstrated. 14C-Ipriflavone was eliminated mostly as metabolites within 48 and 72 h, respectively, in rats and dogs. Rats excreted more 14C in urine than in feces, whereas the reverse was noted in dogs. Biliary excretion and reabsorption of 14C were also obvious in both animals.

Animals↗
PubMed1984

Rat-plasma metabolites of ciglitazone, a new antidiabetic agent.

The rat-plasma metabolites of ciglitazone, a new antidiabetic agent, were characterized by g.l.c.-mass spectrometry as follows: the 2'-, cis-3'-, trans-3'-, cis-4'- and trans-4'-hydroxycyclohexyl derivatives, and 3'- and 4'-oxocyclohexyl derivatives. The 2'-hydroxycyclohexyl derivative contains cis- and/or trans-isomers (unresolved). Three other metabolites, which were postulated to be dihydroxy derivatives of ciglitazone, were also detected in the plasma. All monohydroxy and monoketo metabolites showed hypoglycaemic and hypotriglyceridemic activities in genetically obese-diabetic mice. These results suggest that the pharmacological activities of ciglitazone are due, at least partly, to the metabolites.

Animals↗
PubMed1984

Disposition in rats and dogs of ciglitazone, a new antidiabetic agent.

Oral 14C-ciglitazone was well absorbed by rats to give a maximum plasma level at two hours and an apparent half-life of 4.9 h. In dogs, the plasma level of the compound, after oral administration, reached a plateau at one hour, persisted till ten hours and then declined with a half-life of 23.5 h. In rats, plasma levels of metabolites were higher than those of unchanged ciglitazone, whereas the reverse was noted in dogs. Plasma metabolites were the monohydroxycyclohexyl derivatives (mono-ol) and monoketocyclohexyl derivatives (mono-oxo), together with other components consisting largely of dihydroxycyclohexyl derivatives (di-ol) and unknown polar metabolites. Metabolites found in rats were pharmacologically active trans-4'-ol, 3'-ol, 4'-oxo, cis-4'-ol, 3'-oxo and 2'-ol in the decreasing order listed, and those in dogs were 3'- and/or 4'-ols. Ciglitazone was highly bound to plasma protein of both animals. After oral administration of 14C-ciglitazone to rats, 14C was widely distributed in tissues, with the highest concn. in the gastrointestinal tract, followed by liver, adipose, plasma, adrenal gland, kidney, pancreas, spinal cord, heart and lung, and the lowest in the brain. The concn. of 14C in erythrocytes of rats and dogs was very low, as was the level of 14C in rat fetuses. Elimination of 14C-ciglitazone was complete within 96 h in rats and 144 h in dogs. In both animals, the dosed 14C was excreted largely in faeces as metabolites, with the remainder appearing in urine. Biliary excretion and reabsorption of 14C were obvious in rats. In both rats and dogs, the major metabolites found in faeces were 3'- and/or 4'-ols and other components derived from bile, and those in urine were other components. On repeated oral administration of 14C-ciglitazone to rats for seven days, no accumulation of 14C occurred in plasma and tissues, and 97.5% of the dose was eliminated from the body within 96 h after the last administration.

Administration, Oral↗
PubMed1984

[Spontaneous speech disturbances in so called transcortical motor aphasia--comparison of 3 cases with the different lesion sites].

So called transcortical motor aphasia (TCMA) is frequently subdivided, because the clinical features and the localization of the lesions are variable. The authors have been attempting to classify TCMA into three types according to the distribution of the lesions, such as Type F 1, Type F 2 and Type F 3. Case 1 N.S. belongs to Type F 1 showing the clinical features of TCMA with bleeding in the territory of the left anterior cerebral artery. Case 2 M.E. belongs to Type F 2 (published case). This case is similar to Luria's dynamic aphasia in its clinical features and results from the lesions including the posterior parts of left middle frontal gyrus. Case 3 N.T. belongs to Type F 3 who recovered from typical Broca aphasia after language training for four years. The case is similar to Goldstein's Type 1 of TCMA in its clinical features. These three cases are compared with regard to the fundamental bases of spontaneous speech disturbance. The items of comparison are as follows; the volume of speech production and the the time taken to start speech, word fluency test, cue effects necessary for the success of sentence constructions grammatical ability. The results are summerized in Table 2. Type F1 shows the most conspicuous defect of spontaneous speech, but no disturbance in grammatical ability. And when the top word of a sentence (a subject word) is given by the examiner, the patient can construct a structurally correct sentence. These findings imply that the spontaneous speech disturbance of Type F 1 is due to a defect of the starting mechanism of speech.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1983

[An autopsy case of transcortical motor aphasia].

An autopsy case of transcortical motor aphasia is presented with a pathology located anterior and superior to the pars opercularis of the left inferior frontal gyrus. Case H. Y. A 60-year-old right-handed man. On Nov. 14, 1978, the patient had surgery to remove cerebral hematoma in the left frontal lobe. In the neuropsychological examination before the operation, he had shown the clinical features of transcortical motor aphasia characterized by good comprehension of language, preserved repetition, and spontaneous speech disorder. In this stage, it was supposed that the underlying disturbance of spontaneous speech was due to the disabilities of contextual constructions of sentences rather than the lack of speech initiation. Following the operation, however, spontaneous speech disappeared completely for several days. At the same time, the patient showed problems in comprehension, reading, writing and confrontation naming as well as symptoms of disorientation, pathological inertia and 'loss of initiation' in the psychomotor domain. During the following three months, however, the patient did show slight improvement, except for contextual sentence constructions and pathological inertia when taking the complex animal drawing test. In his terminal stages, the clinical symptoms could be summarized as transcortical motor aphasia and mild frontal lobe syndrome. On March 1, 1979, the patient died of Hamman-Rich syndrome. Postmortem examination: The brain weighed 1294 gm. The external observation of the brain disclosed the linear tissue defect, about 15 mm in length and 10 mm in width, along the radial sulcus of the pars triangularis of the left inferior frontal gyrus.(ABSTRACT TRUNCATED AT 250 WORDS)

Aphasia↗
PubMed1979

Recovery from alexia without agraphia: report of an autopsy.

The patient is a 58-year-old Japanese teacher of German literature who suffered twice from cerebrovascular accidents, showing alexia without agraphia. Pathological examination showed an old infarct in the posterior two-thirds of the fusiform and almost the whole lingual gyrus, involving the posterior border of the parahippocampal gyrus in the left hemisphere. The left cuneus and the calcarine cortex were preserved. There was degeneration of the lower third of the splenium of the corpus callosum, extending to its occipital radiation and tapetum on both sides. Comparing clinico-pathological findings of the 31 known autopsy cases, it was proposed that the lesion of the left spleno-lingual system produces alexia without agraphia but it may ameliorate. In addition, when spleno-cuneate system is also involved alexia becomes persistent and it may accompany object agnosia or optic aphasia.

Agraphia↗