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  inhibitory effect
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    Terephthalic Acid Induced Bladder Lesion
    对苯二甲酸致膀胱损伤作用的研究
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    3.Potassium antimony tartrate on the isolated rabbit heart and vessels
    锑剂对于循环系的药理 3.酒石酸锑钾对于离体心血管的作用
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  inhibitory effect
Among a total of 38 glycosyl ureas, 2 showed more than 50% inhibitory effect.
      
Among a total of 66 glycosyl ureas/ thioureas and glycopeptidyl ureas, 3 showed more than 50% stimulatory effect whereas 2 showed more than 50% inhibitory effect.
      
Increased inhibitory effect of methanol extracts over berberine demonstrates the occurrence of other cytotoxic principles along with main active principle berberine or other factors enhancing the cytotoxic effect of berberine.
      
However, no significant inhibitory effect was obtained on superoxide anion formation.
      
Of all the groups, the 5 × 1015 ion/cm2 dosage group yielded the best effect, whereas the 1 × 1017/cm2 dosage group showed an evident inhibitory effect of ion implantation on the germination and growth of the sesame seeds.
      
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(1) Sodium salt of reduced codehydrogenase I has been obtained in good yield as a dry powder from codehydrogenase I by reduction with alcohol and alcohol dehydrogenase. This preparation was stable for at least 5 months when kept dry at -15℃. (2) The properties of the particle-bound codehydrogenase I cytochrome reductase system in heart muscle preparation were found to differ considerably from those of the soluble enzyme as obtained by Mahler et al. Among other things, the affinity for cytochrome c of the particle-bound...

(1) Sodium salt of reduced codehydrogenase I has been obtained in good yield as a dry powder from codehydrogenase I by reduction with alcohol and alcohol dehydrogenase. This preparation was stable for at least 5 months when kept dry at -15℃. (2) The properties of the particle-bound codehydrogenase I cytochrome reductase system in heart muscle preparation were found to differ considerably from those of the soluble enzyme as obtained by Mahler et al. Among other things, the affinity for cytochrome c of the particle-bound enzyme is much greater than the soluble enzyme. The Michaelis constant for cytochrome c of the former is only one twelfth of that of the latter.(Fig. 2A). (3) With either oxygen or excess cytochrome c as electron acceptor, it was found that the overall activity, in terms of rate of oxygen consumption or cytochrome c reduction, when both succinate and reduced codehydrogenase I were oxidized simultanously, did not represent the sum of the rates of oxidation when these two substrates were separately oxidized but equalled only the faster of the two separate oxidation rates(Fig. 5, Tables 1, 2). If 2,6-dichlorophenol indophenol was used as the electron acceptor, the overall rate of simultaneous oxidation of these two substrates was found to equal exactly the sum of the rates of separate oxidation(Table 3). (4) When either oxygen or excess cytochrome c was used as the electron acceptor, reduced codehydrogenase I and succinate each inhibited the rate of oxidation of the other(Figs 4, 6 & 7). Evidence has been presented to show that the inhibition of succinate oxidation by reduced codehydrogenase I is not due to the accumulation of oxaloacetate. (5) When malonate was also added to the reaction mixture, succinate no longer produced any inhibition of the oxidation of reduced codehydrogenase I(Fig. 8). (6) It is therefore concluded that in heart muscle preparation both succinate and reduced codehydrogenase I are oxidized by cytochrome c through a common, velocity limiting factor. This is in accordance with the view previously reached by some workers from studies on the action of certain inhibitors. However, it should be noted that in our experiments no agents which might produce any conceivable change in the colloidal structure of the enzyme system has been employed. (7) It should be emphasized that our results clearly show that great caution must be exercised in drawing conslusion on the role an enzyme might play in a complex enzyme system from studies of the properties of a solubilized enzyme. (8) It is believed that the competition of two enzyme systems for a common linking factor as demonstrated in this report has provided a new method for studies on the mutual relations of two or more enzyme systems.

(一)本報告提供了一個從輔酶Ⅰ,用酶還原法製備還原輔酶Ⅰ的方法。我們所製得的還原輔酶Ⅰ鈉鹽乾粉,可以在低温保存數月而不被氧化。 (二)與心肌製劑中顆粒相結合的輔酶Ⅰ細胞色素還原酶系,和用乙醇抽出的水溶性的輔酶Ⅰ細胞色素還原酶的性質頗不相同。其中比較重要的不同點是對於細胞色素c的親力,前者遠大於後者,其米氏常數僅約為後者的十二分之一。 (三)用一心肌顆粒製劑作為材料,無論用氧或過量之細胞色素c作為氫受體,還原輔酶Ⅰ與琥珀酸同時氧化時的總速度,不等於二者分別氧化時速度之和,而僅等於其中氧化較快者單獨氧化時之速度。但如用[2,6]二氯靛酚作為氫受體時,二者共同氧化時之總速度完全等於二者分別氧化時速度的和。 (四)當用氧或過量之細胞色素c作為氫受體時,琥珀酸與還原輔酶Ⅰ能彼此互相抑制對方氧化的速度。有足夠的實驗材料說明,還原輔酶Ⅰ對於琥珀酸氧化的抑制,不是由於草醯乙酸聚集的緣故。 (五)如果在反應混合物中同時含有琥珀酸脫氫酶的專一抑制劑,丙二酸,則琥珀酸對於還原輔酶Ⅰ氧化作用的抑制即被解除。 (六)根據以上的實驗結果,可以認為,還原輔酶Ⅰ及琥珀酸先通過一個共同的因子與細胞色素c作用。這個共同的...

(一)本報告提供了一個從輔酶Ⅰ,用酶還原法製備還原輔酶Ⅰ的方法。我們所製得的還原輔酶Ⅰ鈉鹽乾粉,可以在低温保存數月而不被氧化。 (二)與心肌製劑中顆粒相結合的輔酶Ⅰ細胞色素還原酶系,和用乙醇抽出的水溶性的輔酶Ⅰ細胞色素還原酶的性質頗不相同。其中比較重要的不同點是對於細胞色素c的親力,前者遠大於後者,其米氏常數僅約為後者的十二分之一。 (三)用一心肌顆粒製劑作為材料,無論用氧或過量之細胞色素c作為氫受體,還原輔酶Ⅰ與琥珀酸同時氧化時的總速度,不等於二者分別氧化時速度之和,而僅等於其中氧化較快者單獨氧化時之速度。但如用[2,6]二氯靛酚作為氫受體時,二者共同氧化時之總速度完全等於二者分別氧化時速度的和。 (四)當用氧或過量之細胞色素c作為氫受體時,琥珀酸與還原輔酶Ⅰ能彼此互相抑制對方氧化的速度。有足夠的實驗材料說明,還原輔酶Ⅰ對於琥珀酸氧化的抑制,不是由於草醯乙酸聚集的緣故。 (五)如果在反應混合物中同時含有琥珀酸脫氫酶的專一抑制劑,丙二酸,則琥珀酸對於還原輔酶Ⅰ氧化作用的抑制即被解除。 (六)根據以上的實驗結果,可以認為,還原輔酶Ⅰ及琥珀酸先通過一個共同的因子與細胞色素c作用。這個共同的因子在一般情形之下,也是這兩個酶系統的速度限制因子。應該指出在我們的實驗中,並未使用任何可能影響酶系統結構的條件,因此我們的結果是在一個比較接近於生理狀態的情形之下獲得的。 (七)應該着重指出,從本報告的結果可以看到,一個用人為的方法從複雜酶系上溶解下來的酶的性質,有時並不能代表這個酶在有組織的酶系統中的真實情况。 (八)我們相信,本報告所說明的兩酶系競爭一個共同因子的一些現象,將为研究複雜酶系之間的相互關係,提供一個新的方法。

Observations were made to compare the effect of HCl introduced into the small intestine of dogs on pancreatic secretion in the following three conditions: (1) Acute experiments with barbiturates(pentothal sodium or pentobarbital sodium) as an(?)sthesia; (2) Chronic experimental dogs with Thomas pancreatic fistula; (3) Chronic dogs in(2) an(?)sthetized by means of the same barbiturates as in the acute experiments. The results indicated that in the acute experiments, the latent period of pancreatic secretion was...

Observations were made to compare the effect of HCl introduced into the small intestine of dogs on pancreatic secretion in the following three conditions: (1) Acute experiments with barbiturates(pentothal sodium or pentobarbital sodium) as an(?)sthesia; (2) Chronic experimental dogs with Thomas pancreatic fistula; (3) Chronic dogs in(2) an(?)sthetized by means of the same barbiturates as in the acute experiments. The results indicated that in the acute experiments, the latent period of pancreatic secretion was about 3-5 minutes and the amount secreted was usually below 20 drops in the first 30 minutes after the introduction of the acid. But in the case of chronic experiments, the results were quite different. The latent period was shorter, usually less than 2 minutes and the amount of pancreatic secretion was usually 10 times as much as in the acute experiments. Moreover, the pancreatic secretion of the chronic fistula dogs was not changed either in latent period or in amount when under the barbiturate an(?)sthesia. From the above results, it is quite natural to assume that the influence of the barbiturate an(?)sthetics, pentothal sodium and pentobarbital sodium on pancreatic secretion induced by HCl in the intestine of dogs is negligible. The great difference in the pancreatic secretion between the acute and the chronic experiments might, therefore, be due to the operative trauma which is unavoidable in acute experiments. Another observation was made to determine the effect of atropine on pancreatic secretion induced by HCl in chronic fistula dogs. The result showed that atropine distinctly reduced the response of pancreas to the acid. The latent period was increased and the amount of pancreatic secretion was decreased as compared with the result obtained in normal chronic fistula dogs. Hence it is quite suggestive that there might exist a nervous component in the mechanism of pancreatic secretion induced by HCl in the small intestine. We wish to express our gratitude to Comrade for his valuable advice and to professors T. C. Shen and T. F. Liu for their encouragement throughout this work.

本實驗比較急性實驗狗、慢性胰瘻狗和經過麻醉的慢性胰屢狗對於鹽酸注入小腸所引起的胰液分泌量和潛伏期,結果證明: (1)在急性實驗情况下,狗胰腺對鹽酸刺激小腸所引起的胰液分泌量遠較在慢性實驗時為少,且潛伏期較長。 (2)巴比妥類麻醉劑:硫賁妥鈉(sodium pentothal)和戊烷巴比妥鈉(sodiumpentobarbital)對鹽酸所引起的胰液分泌量及潛伏期影響極微。 (3)在急性實驗情况下,由鹽酸所引起的胰液分泌量的減少和潛伏期的加長,似乎不是由於巴比妥類麻醉劑的作用,而可能是由於手術創傷的影響。 (4)注射阿托平後,胰腺對於鹽酸刺激小腸所引起的反應顯著减小,故推测在鹽酸引起胰液分泌的機制中可能有神經反射作用的參與。本工作在进行過程中,承蘇聯專家同志親切地給予指導,并承沈(?)淇、劉曾復二教授关懷和支持,(?)此誌謝。

Although the occurence of a coenzyme I-independant, particle-bound α-glycerophosphate dehydrogenase in skeletal muscle of higher animals has long been recognized, little is known about its relation to the cytochrome system. Green has found that it is linked to cytochrome c but details of the electron transporting pathway has remained obscure. This problem has now been studied using the method of simultaneous action of two or more enzyme systems as described previously. Enzyme preparation obtained from thoroughly...

Although the occurence of a coenzyme I-independant, particle-bound α-glycerophosphate dehydrogenase in skeletal muscle of higher animals has long been recognized, little is known about its relation to the cytochrome system. Green has found that it is linked to cytochrome c but details of the electron transporting pathway has remained obscure. This problem has now been studied using the method of simultaneous action of two or more enzyme systems as described previously. Enzyme preparation obtained from thoroughly washed rabbit muscle mince has been employed in the present investigation. It has been found that in the presence of the rabbit muscle enzyme preparation, succinate and α-glycerophosphate each interferes with the rate of oxidation of the other when they are oxidized simultaneously. The inhibition of α-glycerophosphate oxidase by succinate can be reversed by the addition of pyrophosphate, a powerful inhibitor of succinic dehydrogenase. With cytochrome c as electron acceptor, the overall rate of simultaneous oxidation of α-glycerophosphate, succinate and reduced coenzyme I (CoIH) does not represent the sum of the rates of their separate oxidation, but corresponds only to the highest of the three rates, i.e. the rate of oxidation of CoIH. It is, therefore, believed that the α-glycerophosphate-, succinate- and CoIH-cytochrome c reductase systems have a common, velocity limiting electron carrier which is most probably the linking factor first proposed by Slater. In agreement with this conclusion, the α-glycerophosphate oxidase of rabbit muscle preparation has been found to be sensitive to the action of 2,3-dimercaptopropanol. Using 2,6-dichlorophenolindophenol, as acceptor, the overall rate of the simultaneous oxidation of succinate and α-glycerophosphate equals exacdy to the sum of the rates of their separate oxidation. Similar results have also been obtained even in presence of phenylurethane, which markedly inhibits the activity of succinic dehydrogenase and does not affect the activity of α-glycerophosphate dehydrogenase. These facts suggest that cytochrome b is not involved in the oxidation of α-glycerophosphate in rabbit muscle preparation. The pathway of hydrogen or electron transfer of the particulate α-glycerophosphate oxidase system may, therefore, be represented as follow: (See also Fig. 4)

(一) 在經徹底冲洗的兔骨骼肌製劑中,[L-α]甘油磷酸和琥珀酸的氧化彼此干涉。琥珀酸對[L-α]甘油磷酸氧化的抑制作用能因加入抑制琥珀酸脫氫酶的焦磷酸而解除。 (二) 當用細胞色素c作受體時[L-α]甘油磷酸,還原輔酶I和琥珀酸三者同時氧化時總氧化速度僅相當其中氧化速度最高者即還原輔酶I單獨氧化的速度。[L-α]甘油磷酸氧化酶系也因[2,3]二氫硫基丙醇的處理而失效。 (三) 當用[2,6]二氯酚靛酚作受體時[L-α]甘油磷酸和琥珀酸同時氧化時速度完全等於二底料單獨氧化時速度的和。[L-α]甘油磷酸的氧化不受苯代氨甲酸乙酯的影響。 (四) 本文結果說明[L-α]甘油磷酸的氧化不通過細胞色素b而通過中間因子和細胞色素c連接。

 
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