宮崎 良文

To investigate an effect of inhalation of Taiwan Hinoki ( Chamaecyparis taiwanensis Matum. et Suzuki ) wood oil of 3 different concentrations on mood, we measured pupillary light reflex, blood pressure, R - R interval, and performance indicating changes in mood. Six female students were used as subjects of the study. Control experiments were conducted similarly without odor. The results indicated that 1) maximum constriction acceleration of the pupil increased and blood pressure decreased after inhalation of the Taiwan Hinoki oil, 2) the speed of performing " letter cancellation " increased after inhalation of Taiwan Hinoki oil, and 3) maximum constriction acceleration of the pupil increased and blood pressure decreased along with increase in the intensity of the odor. We concluded that inhalation of the Taiwan Hinoki oil caused a physiological change and the change differed by the intensity of the odor.

森林環境学の立場から生気象学の思想について論じた.健康と快適性が重要な視点となる.特に, 快適性に関しては, 健康と安全性の方が優先されることは当然であるが, 今, 生気象学の中にあって重要な位置を占めている.本論文においては, 第1に森林環境と生気象学のかかわりについて論じた.第2に今後の重要な視点となる快適性について考察した.さらに, 第3に森林環境が人の快適性や健康に及ぼす影響に関して我々の報告を中心に紹介した.学際的な学問である生気象学において, 森林環境と人の関係を健康と快適性の観点から解明することが, 今後, 重要である.

ヒノキ精油成分カジネンが腎臓, 肺, 副腎, 精巣におけるチトクロームP-450の組織内分布に及ぼす影響をフェノバルビタール (PB) 誘導分子種とメチルコラントレン (MC) 誘導分子種に分けて調べた.ウィスター系, 雄のラットを使い, 抗ラットPB-P-450および抗ラットMC-P-450家兎血清を用いて免疫組織学的に検索した.その結果, 第1に肺, 副腎, 精巣の各臓器でPB誘導分子種が増加していること, 第2にこれらの各臓器においてはMC誘導分子種は増加していないこと, 第3に腎臓ではPBおよびMC誘導分子種は増加していないことが明らかになった.

In order to investigate the circadian variations in acute toxicity of trichloroethylene (TRI), TRI (1.2 g/kg weight) or saline was injected intraperitoneally in a total of 88 male Wistar rats at four circadian stages (03.00,09.00,15.00,and 21.00:hr.min) under two different lighting regimens of a 12:12 hr light-dark cycle (LD; light from 06.00 to 18.00) and of constant darkness (DD). Circadian variations in TRI toxicity were confirmed in both LD and DD. The toxicity of TRI evaluated by the increase in glutamic-pyruvate transaminase activity (GPT) was greatest when injected at 09.00 in LD while at 21.00 in DD. The increases in blood urea nitrogen, serum total cholesterol and triglyceride concentrations reached peaks when injected at 09.00 in LD and at 03.00 in DD. The circadian variations in serum trichloroethanol concentration were very similar to those in GPT in both LD and DD, showing a significant correlation (p < 0.05). The present study revealed that circadian variations in TRI toxicity existed in LD and that these variations persisted in a free-running condition. The peak phase of TRI toxicity was located in a trough phase (09.00) in LD and in a peak phase (21.00 or 03.00) in DD of temperature rhythm. Thus, the phase relationship changed in DD, showing a desynchronization between TRI toxicity rhythm and temperature rhythm, which is an unusual phenomenon. This means that an unexpected potentiation of TRI toxicity during active phase which is not a critical phase in a well-synchronized state could occur in a free-running condition. © 1990.

肝臓のミクロゾームの数種のチトクロームP-450分子種に及ぼすヒノキ (Chamaecyparis obtusa) 材の精油の影響を, オスのウィスター系ラットを用いて調べた.その結果, 第1に, ヒノキ精油の腹腔内投与 (300mg/kg, ×2) により, P-450の総含量は50%の増加 (p<0.01) を示すこと, 第2に, ウェスタンブロッティングによる免疫化学的定量から, P450 PB-4とPB-5が, 対照に比べ12倍に増加していること, 第3に, P450 MC-5は増加していないことが明らかとなった.これらの分子種の変動は, テストステロン水酸化活性, 7-エトキシクマリン脱エチル化活性, および, HPLCによる溶出パターンから確認された.

寒冷曝露 (4℃) によるチトクロームP-450の肝臓組織内分布の変化について, 抗ラットPB-P-450家兎血清を用いて免疫組織学的に検討した.<br /> PB-P-450を多く含む肝細胞は, 24℃飼育ラットでは肝小葉内中心静脈の周囲に局在していたが, 寒冷曝露4週間ラットでは肝小葉全体に分布していた.この曝露4週群におけるPB-P-450陽性細胞において, その反応は強陽性であり, 細胞質内のPB-P-450陽性顆粒も, 対照群に比べ密に認められた.寒冷曝露3週間ラットではPB-P-450分布は中間的な変化を示し, 寒冷曝露1, 2週間ラットでは, 24℃飼育ラットと比べ免疫組織学的に有意な変化は認められなかった.<br /> 寒冷曝露4週間ラットでは生化学的方法にて測定されるアミノピリン代謝速度の上昇を認め, この結果はPB-P-450陽性の肝細胞数の増加, 細胞内のPB-P-450陽性顆粒の密度の増加と対応しているものと考えられた.

©,The interaction of cytochrome P-450 and dichloromethane (DCM) was investigated spectrophotometrically in the perfused rat liver. DCM bound to cytochrome P-450 and showed a type I spectral change, with a peak at 450 nm. The peak at 450 nm was developed by addition of exogenous carbon monoxide (CO) to the perfusate. By examining the pattern of the spectral change, we concluded that CO formed during DCM metabolism by cytochrome P-450 bound to cytochrome P-450 in the perfused liver.

1. The action of 1,1,1-trichloroethane (1,1,1-TCE) on cytochrome P-450-dependent mixed-function oxidation by rat liver microsomes was studied by determination of the rates of O2 consumption, H2O2 production, and 1,1,1-TCE metabolism, and from the spectral change in cytochrome P-450. 2. 1,1,1-TCE caused increases in the rate of O2 consumption, and H2O2 production, although metabolism of 1,1,1-TCE was minimal. The stoichiometry of the rate of metabolism of 1,1,1-TCE to the increase in the rate of O2 consumption was about 0·011. The increase in O2 consumption and the production of H2O2 did not occur in microsomes treated with SKandF 525-A. 3. Spectral studies indicated that 1,1,1-TCE bound to cytochrome P-450 and showed a type I spectral change. 4. The addition of NADH with NADPH in the reaction medium enhanced the increase in O2 consumption caused by 1,1,1-TCE, whereas it did not change the rate of H2O2 production. 5. There was no increase in the formation of thiobarbituric acid reactive substances in the reaction medium incubated with 1,1,1-TCE. 6. It was concluded that 1,1,1-TCE had an uncoupling effect on the cytochrome P-450-dependent mixed-function oxidation system. © 1988 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.

The interaction of nitrite with catalase was investigated spectrophotometrically in the perfused rat liver. Real-time spectral changes were obtained using a reflectance scanning spectrophotometer in the liver perfused with a haemoglobin-free medium in a non-recirculating system. Administration of sodium nitrite caused a specific pattern of spectral change indicating the decomposition of catalase compound I to free catalase. The spectral change due to the interaction with nitrite did not occur during potassium cyanide or ethanol infusion, nor in the aminotriazole-pretreated rat liver. The spectral change was observed at concentrations of nitrite in the perfusate over 0.01 mm, and the K0.5 value (the concentration producing half the maximum spectral change) was 0.06 mm. It was concluded that relatively low concentrations of nitrite caused decomposition of catalase compound I in the physiologically functioning liver cell. © 1988.

The metabolism of chloral hydrate (CH) under anoxic conditions was investigated in the non-recirculating, hemoglobin-free liver perfusion system. CH uptake in the anoxic liver decreased to about 80% of that in the oxygen-supplied liver. The reduction of CH to trichloroethanol (TCE) increased and the oxidation of CH to trichloroacetic acid (TCA) decreased. The TCE/TCA ratio increased however, the total trichloro compounds, that is TCE and TCA, were not significantly altered by anoxia. Though approximate 14% of the CH infused into the oxygen-supplied liver was changed to substances other than TCE or TCA, the unknown part was a very small portion in the anoxic liver. The decrease in CH uptake, by the anoxic liver, is thought to be equivalent to the decrease of the unknown metabolites. The TCE/TCA ratio under anoxia was also altered by pyruvate or lactate infusion. © 1988.

©,Chloral hydrate (CH), an intermediate metabolite of trichloroethylene, is reduced to trichloroethanol (TCE) by alcohol dehydrogenase and aldehyde reductase, and is also oxidized to trichloroacetic acid (TCA) by the nicotinamide adenine dinucleotide (NAD)‐dependent enzyme, CH dehydrogenase. Alcohol dehydrogenase requires reduced NAD (NADH), aldehyde reductase requires reduced nicotinamide adenine dinucleotide phosphate (NADPH) and CH dehydrogenase requires NAD to complete the reaction. It is unclear which reaction is predominant at the physiological redox level in intact liver cells. To study this question, we perfused the livers of well‐fed rats with Krebs‐Ringer buffer solution containing 0.1 mM pyruvate/1.0 mM lactate. The levels of TCE and TCA in the effluent were measured by gas chromatography, and the fluorescence of reduced pyridine nucleotides was measured with a surface fluorometer. When a low concentration (below 0.25 mM) of CH was administered, more TCA than TCE was produced. When a high concentration of CH was administered (over 0.5 mM), TCE production was greater. Reduced pyridine nucleotides decreased inversely with the CH concentration. Even at low CH concentrations, pyridine nucleotides were not reduced. When 10 mM lactate was added to the perfusate in order to reduce the pyridine nucleotides in the liver cells, the TCE/TCA ratio increased. On the other hand, the TCE/TCA ratio tended to fall following the addition of 5.0 mM pyruvate. In conclusion, the TCE/TCA ratio was altered according to the concentration of CH, and to the redox level of pyridine nucleotides in the liver.

Changes in the hepatic cytochrome P-450-dependent drug-metabolizing system were studied in perfused livers obtained from cold-acclimated male Wistar rats after 30 days of cold exposure (4‡C) when using hexobarbital as a substrate. In fasted animals the cold-acclimated rats showed higher levels of hexobarbital metabolic rates compared to control rats, but there was no significant difference in fed animals. The maximum rates of hexobarbital metabolism produced by xylitol perfusion were also significantly higher in the perfused liver of cold-acclimated rats. It was concluded that the function of the cytochrome P-450 system for hexobarbital in cold-acclimated rats changed due to both an increase in the activity of the cytochrome P-450 system and to changes in regulation of the cytochrome P-450 system by the supply of reducing equivalents. © 1986 Swets &amp; Zeitlinger.

Interaction of Trichloroethane Isomers with Cytochrome P-450 in the Perfused Rat Liver. TAKANO, T., MIYAZAKI, Y., and MOTOHASHI, Y. (1985). Fundam. Appl. Toxicol. 5, 353-360. The real-time interactions of 1,1,1-trichloroethane (TCE) and 1,1,2-TCE with cytochrome P-450 were observed using in vivo optical methods to measure the spectral changes of cytochrome P-450 and the reduction-oxidation transition of pyridine nucleotides in the perfused liver of rats treated with phenobarbital. Changes in oxygen consumption and TCE uptake were also measured. The spectral changes of cytochrome P-450 indicated that both TCE isomers bound to low spin (substrate free) ferric cytochrome P-450 and formed a high spin (substrate complexed) form. However, 1,1,1-TCE bound more tightly to cytochrome P450 and seemed to be only slowly metabolized compared to 1,1,2-TCE. The stoichiometry of the change in oxygen consumption rate to the change in 1,1,1-TCE uptake rate ranged between 5/1, and 9/1, whereas that of 1,1,2-TCE was 1.4 to 2.0. Decreases in reduced pyridine nucleotides associated with TCE administration were significantly larger with 1,1,1-TCE than with 1,1,2-TCE. The inhibitory effect of 1,1,1-TCE on hexobarbital metabolism in the perfused liver was greater than that of 1,1,2-TCE. Considering our previous data indicating that TCE did not stimulate mitochondrial respiration, it is postulated that the far higher amount of oxygen consumption associated with the binding of 1,1,1-TCE to cytochrome P450 than the amount which was necessary to mixed-function oxidation of this compound was due to an uncoupling effect of 1,1,1 -TCE on the mixed-function oxidase system. © 1985 Copyright 1985 by the Society of Texicology.