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Anisylidenenitromethane의 친핵성 가수분해 반응의 반응기구
박옥현,임미재 梨花女子大學校 韓國生活科學硏究院 1973 韓國生活科學硏究院 論叢 Vol.11 No.-
Anisylidenenitromethane (ANM)의 친핵성 가수분해 반응의 반응속도 상수를 여러 pH에서 구하였고 이 반응메카니즘에 잘 적용되는 전체 반응속도식을 구하였다. 이 반응속도식에서 산성쪽 반응메카니즘과 염기성쪽 반응메카니즘이 서로 다르다는 것을 알았다. 즉 산성쪽의 가수분해반응은 ANM에 물분자가 먼저 첨가됨으로서 반응이 시작되나 염기성쪽에서는 hydroxide ion의 첨가에 의하여 반응이 시작된다. 그러나 Mechael 반응에 따르지 않고 복잡하다. 왜냐하면 ANM이 강염기용매에서는 약산으로 작용하여 해리가 이루어지기 때문이다. 따라서 acid dissociation constant (K_a)로 고려해야 하므로 pH 11 이상에서는 rate contant가 일정함을 볼 수 있다. The rate-constants of the nucleophilic hydrolysis of anisylidenenitromethane (ANM) were determined at various pH and a rate-equation that could be well applied to the all range of pH were also obtained. This rate-equation shows that the mechanism of the reaction in acidic media is different from that in basic media: The reaction of hydrolysis in acid media is started by addition of water molecule, but that in basic media is started by addition of hydroxyl ion. However it is not involved in Michael reaction, because ANM in strong basic media behaves as weak acid and acid dissociation costant (Ka) of ANM should be considered at the rate-equation. Here the rate constants keep the same when above pH 11 it is.
ω-nitro-2-vinylthiophene의 친핵성 가수분해 반응메카니즘의 반응속도론적 연구
朴玉鉉,吳容玉,任美宰 梨花女子大學校 韓國生活科學硏究院 1974 韓國生活科學硏究院 論叢 Vol.13 No.-
The rats constants of the nucleophilic hudrolysis of ω-nitro-2-vinyl thiophene (NVT) were determined at vrious pH and the rate equations were obtained that can be applied to the whole range of pH. From these rate equations, the mechanisms of the reaction are different in acidic and basic media. The reaction of hydrolysis in acid media is started by the addition of the hydroxide ion.
김선영,김상진,김병주,나소영,정성모,임미재,김우현 생화학분자생물학회 2006 Experimental and molecular medicine Vol.38 No.5
Doxorubicin (DOX) is one of the most potent anticancer drugs and induces acute cardiac arrhythmias and chronic cumulative cardiomyopathy. Though DOX-induced cardiotoxicity is known to be caused mainly by ROS generation, a disturbance of Ca2+ homeostasis is also implicated one of the cardiotoxic mechanisms. In this study, a molecular basis of DOX-induced modulation of intracellular Ca2+ concentration ([Ca2+]i) was investigated. Treatment of adult rat cardiomyocytes with DOX increased [Ca2+]i irrespectively of extracellular Ca2+, indicating DOX-mediated Ca2+ release from intracellular Ca2+ stores. The DOX-induced Ca2+ increase was slowly processed and sustained. The Ca2+ increase was inhibited by pretreatment with a sarcoplasmic reticulum (SR) Ca2+ channel blocker, ryanodine or dantrolene, and an antioxidant, α-lipoic acid or α-tocopherol. DOX-induced ROS generation was observed immediately after DOX treatment and increased in a time-dependent manner. The ROS production was significantly reduced by the pretreatment of the SR Ca2+ channel blockers and the antioxidants. Moreover, DOX-mediated activation of caspase-3 was significantly inhibited by the Ca2+ channel blockers and α-lipoic acid but not α-tocopherol. In addition, cotreatment of ryanodine with α-lipoic acid resulted in further inhibition of the casapse-3 activity. These results demonstrate that DOX-mediated ROS opens ryanodine receptor, resulting in an increase in [Ca2+]i and that the increased [Ca2+]i induces ROS production. These observations also suggest that DOX/ROS-induced increase of [Ca2+]i plays a critical role in damage of cardiomyocytes.