Gutierrez Correa J, Stoppani A O
Bioenergetics Research Centre, School of Medicine, University of Buenos Aires, Argentina.
Free Radic Res Commun. 1993;19(5):303-14. doi: 10.3109/10715769309056519.
Fe(II)- and Co(II)-Fenton systems (FS) inactivated the lipoamide reductase activity but not the diaphorase activity of pig-heart lipoamide dehydrogenase (LADH). The Co(II) system was the more effective as LADH inhibitor. Phosphate ions enhanced the Fe(II)-FS activity. EDTA, DETAPAC, DL-histidine, DL-cysteine, glutathione, DL-dithiothreitol, DL-lipoamide, DL-thioctic acid, bathophenthroline, trypanothione and ATP, but not ADP or AMP, prevented LADH inactivation. Reduced disulfide compounds were more effective protectors than the parent compounds. Mg ions counteracted ATP protective action. Glutathione and DL-dithiothreitol partially restored the lipoamide dehydrogenase activity of the Fe(II)-FS-inhibited LADH. DL-histidine exerted a similar action on the Co(II)-FS-inhibited enzyme. Ethanol, mannitol and benzoate did not prevent LADH inactivation by the assayed Fenton systems and, accordingly, it is postulated that site-specific generated HO. radicals were responsible for LADH inactivation. With the Co(II)-FS, oxygen reactive species other than HO., might contribute to LADH inactivation.
亚铁（II）和钴（II）-芬顿体系（FS）可使猪心脂酰胺脱氢酶（LADH）的脂酰胺还原酶活性失活，但不影响其黄递酶活性。钴（II）体系作为LADH抑制剂更有效。磷酸根离子可增强亚铁（II）-FS的活性。乙二胺四乙酸（EDTA）、二乙基三胺五乙酸（DETAPAC）、DL-组氨酸、DL-半胱氨酸、谷胱甘肽、DL-二硫苏糖醇、DL-脂酰胺、DL-硫辛酸、bathophenthroline、锥虫噻唑啉和三磷酸腺苷（ATP），但不是二磷酸腺苷（ADP）或一磷酸腺苷（AMP），可防止LADH失活。还原型二硫化合物作为保护剂比母体化合物更有效。镁离子可抵消ATP的保护作用。谷胱甘肽和DL-二硫苏糖醇可部分恢复被亚铁（II）-FS抑制的LADH的脂酰胺脱氢酶活性。DL-组氨酸对被钴（II）-FS抑制的酶有类似作用。乙醇、甘露醇和苯甲酸盐不能防止所检测的芬顿体系使LADH失活，因此推测位点特异性产生的羟基自由基（HO·）是导致LADH失活的原因。对于钴（II）-FS，除HO·之外的氧活性物种可能也参与了LADH的失活过程。
