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アブストラクト（21巻2号：神奈川歯学）
Japanese
| Title ： | アチドーシスの咬筋カルシウム輸送におよぼす影響とその機構 |
|---|---|
| Subtitle ： | 原著 |
| Authors ： | 河野治夫, 伊藤春生 |
| Authors（kana） ： | |
| Organization ： | 神奈川歯科大学歯科薬理学教室 |
| Journal ： | 神奈川歯学 |
| Volume ： | 21 |
| Number ： | 2 |
| Page ： | 176-189 |
| Year/Month ： | 1986 / 9 |
| Article ： | 原著 |
| Publisher ： | 神奈川歯科大学学会 |
| Abstract ： | 「緒言」虚血による嫌気性代謝の促進が, 同時に解糖系反応を促進させ, その結果H+の増加をもたらすことはよく知られている. このH+の蓄積は細胞内pHの低下を導くが, これと併行して虚血時には, 組織酸素濃度の低下のため還元反応が促進する. このような条件下では, 1価の酸素還元反応がおこりやすく, superoxide anionや他のfree radicalが産生される. 虚血時に産生されたfree radicalは, 細胞膜リン脂質の不飽和脂肪酸と容易に相互反応する. 一方, prostaglandinは, 外傷, 神経刺激, 低酸素状態など種々の刺激に反応して細胞膜リン脂質や脂肪酸から合成される. Okabe et al. は, このprostaglandin合成過程の中間代謝物であるendoperoxide G2からendoperoxide H2への酵素的変換時に発生するfree radicalが, 分離咬筋小胞体 (SR) のcalcium輸送を脂質過酸化反応を介して障害する可能性を示唆している. |
| Practice ： | 歯科学 |
| Keywords ： | アチドーシス, カルシウム輸送, フリー・ラジカル |
English
| Title ： | Mechanism of The Effect of Acidosis on Masseter Muscle Calcium Transport |
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| Subtitle ： | |
| Authors ： | Haruo KOHNO, Haruo Ito |
| Authors（kana） ： | |
| Organization ： | Department of Pharmacology, Kanagawa Dental College |
| Journal ： | Kanagawa Shigaku |
| Volume ： | 21 |
| Number ： | 2 |
| Page ： | 176-189 |
| Year/Month ： | 1986 / 9 |
| Article ： | Original article |
| Publisher ： | Kanagawa Odontological Society |
| Abstract ： | [Abstract] : In a previous studies, it has been hypothesized that acidosis and oxygen radicals or the processes that lead to their production may interact in a way such that the damage induced by oxygen radicals may be enhanced by the presence of acidosis. With the implication of both oxygen radical production and a decrease in pH, this study was designed to investigate the possibility that the effect of acidosis on sarcoplasmic reticulum (SR) calcium transport may be mediated by production of oxygen radicals via intermediate steps in the synthesis of prostaglandins (PG) in canine masseter muscle. In vitro, arachidonic acid depressed calcium transport by SR in the homogenate. This effect was inhibited by superoxide dismutase (SOD), a scavenger of the superoxide anion radial (・O-2), at pH 7.0, and by SOD plus d-mannitol, a scavenger of hydroxyl free radical (・OH), at pH 5.5. Indomethacin and 2-aminomethyl-4-tert-butyl-6-propionyl phenol (ONO-3144), a compound known to accelerate the conversion of prostaglandin G2 (PGG2) to PGH2 and scavenge free radicals, inhibited the effect of arachidonic acid at both pH 7.0 and pH 5.5. PGG2, but not PGH2, duplicated the effect of arachidonic acid. The effect of PGG2 on SR function was similar to that of exogenous free radicals generated from the xanthine-xanthine oxidase system. Incubation at pH 5.5, in the absence of an exogenous free-radical generating system, depressed SR calcium transport in the homogenate and in isolated SR. This effect in the homogenate was inhibited by indomethacin or by ONO-3144. At 10-min incubation at pH 5.5, SOD partially and temporarily reversed the depressant effect of acidosis. The addition of SOD plus d-mannitol completely reversed the system. d-Mannitol alone was ineffective. Arachidonic acid was able to mimic these effects of acidosis, except that arachidonic acid further depressed isolated SR calcium transport. It is concluded that acidosis can depress SR calcium transport in the homogenate of masseter muscle by an oxygen-free radical mechanism by the generation of ・O-2 and ・OH, and that significant oxygen radical generation can occur through the cyclooxygenase pathway of arachidonic acid metabolism at an acidotic pH in the cellular environment outside of the SR of the muscle cell. |
| Practice ： | Dentistry |
| Keywords ： |
