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核心技术专利：CN118964589B侵权必究

核心技术专利：CN118964589B侵权必究

Salgueiro-Pagadigorria C L, Kelmer-Bracht A M, Bracht A, Ishii-Iwamoto E L

Department of Biochemistry, University of Maringá, Brazil.

Comp Biochem Physiol C Pharmacol Toxicol Endocrinol. 1996 Jan;113(1):85-91. doi: 10.1016/0742-8413(95)02041-1.

The effects of piroxicam, a nonsteroidal anti-inflammatory drug, on rat liver mitochondria were investigated in order to obtain direct evidence about a possible uncoupling effect, as suggested by a previous work with the perfused rat liver. 2. Piroxicam increased respiration in the absence of exogenous ADP and decreased respiration in the presence of exogenous ADP, the ADP/O ratios and the respiratory control ratios. 3. The ATPase activity of intact mitochondria was increased by piroxicam. With 2,4-dinitrophenol uncoupled mitochondria, inhibition was observed. The ATPase activity of freeze-thawing disrupted mitochondria was insensitive to piroxicam. 4. Swelling driven by the oxidation of several substrates and safranine uptake induced by succinate oxidation were inhibited. 5. The results of this work represent a direct evidence that piroxicam acts as an uncoupler, thus, decreasing mitochondrial ATP generation.

为了获得关于非甾体抗炎药吡罗昔康可能存在的解偶联作用的直接证据，如先前关于灌注大鼠肝脏的研究中所暗示的那样，对大鼠肝脏线粒体进行了研究。2. 吡罗昔康在无外源ADP时增加呼吸作用，而在有外源ADP、ADP/O比值和呼吸控制率时降低呼吸作用。3. 吡罗昔康增加完整线粒体的ATP酶活性。对于2,4-二硝基苯酚解偶联的线粒体，观察到抑制作用。冻融破坏的线粒体的ATP酶活性对吡罗昔康不敏感。4. 由几种底物氧化驱动的肿胀以及琥珀酸氧化诱导的番红摄取受到抑制。5. 这项工作的结果代表了直接证据，即吡罗昔康起解偶联剂的作用，从而减少线粒体ATP的生成。

Salgueiro-Pagadigorria C L, Kelmer-Bracht A M, Bracht A, Ishii-Iwamoto E L

Department of Biochemistry, University of Maringá, Brazil.

Comp Biochem Physiol C Pharmacol Toxicol Endocrinol. 1996 Jan;113(1):85-91. doi: 10.1016/0742-8413(95)02041-1.

The effects of piroxicam, a nonsteroidal anti-inflammatory drug, on rat liver mitochondria were investigated in order to obtain direct evidence about a possible uncoupling effect, as suggested by a previous work with the perfused rat liver. 2. Piroxicam increased respiration in the absence of exogenous ADP and decreased respiration in the presence of exogenous ADP, the ADP/O ratios and the respiratory control ratios. 3. The ATPase activity of intact mitochondria was increased by piroxicam. With 2,4-dinitrophenol uncoupled mitochondria, inhibition was observed. The ATPase activity of freeze-thawing disrupted mitochondria was insensitive to piroxicam. 4. Swelling driven by the oxidation of several substrates and safranine uptake induced by succinate oxidation were inhibited. 5. The results of this work represent a direct evidence that piroxicam acts as an uncoupler, thus, decreasing mitochondrial ATP generation.

为了获得关于非甾体抗炎药吡罗昔康可能存在的解偶联作用的直接证据，如先前关于灌注大鼠肝脏的研究中所暗示的那样，对大鼠肝脏线粒体进行了研究。2. 吡罗昔康在无外源ADP时增加呼吸作用，而在有外源ADP、ADP/O比值和呼吸控制率时降低呼吸作用。3. 吡罗昔康增加完整线粒体的ATP酶活性。对于2,4-二硝基苯酚解偶联的线粒体，观察到抑制作用。冻融破坏的线粒体的ATP酶活性对吡罗昔康不敏感。4. 由几种底物氧化驱动的肿胀以及琥珀酸氧化诱导的番红摄取受到抑制。5. 这项工作的结果代表了直接证据，即吡罗昔康起解偶联剂的作用，从而减少线粒体ATP的生成。