Mitochondrial dysfunction is responsible for the intestinal calcium absorption inhibition induced by menadione

被引:26
|
作者
Marchionatti, Ana M. [1 ]
Perez, Adriana V. [1 ]
Diaz de Barboza, Gabriela E. [1 ]
Pereira, Beatriz M. [1 ]
Tolosa de Talamoni, Nori G. [1 ]
机构
[1] Univ Nacl Cordoba, Fac Ciencias Med, Catedra Bioquim & Biol Mol, Lab Dr Fernando Canas, RA-5000 Cordoba, Argentina
来源
关键词
intestine; mitochondria; menadione; calcium absorption; apoptosis;
D O I
10.1016/j.bbagen.2007.10.020
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Menadione (MEN) inhibits intestinal calcium absorption by a mechanism not completely understood. The aim of this work was to find out the role of mitochondria in this inhibitory mechanism. Hence, normal chicks treated with one i.p. dose of MEN were studied in comparison with controls. Intestinal calcium absorption was measured by the in situ ligated intestinal segment technique. GSH, oxidoreductase activities from the Krebs cycle and enzymes of the antioxidant system were measured in isolated mitochondria. Mitochondrial membrane potential was measured by a flow cytometer technique. DNA fragmentation and cytochrome c localization were determined by immunocytochemistry. Data indicate that in 30 min, MEN decreases intestinal Ca2+ absorption, which returns to the control values after 10 It. GSH was only decreased for half an hour, while the activity of malate dehydrogenase and alpha-ketoglutarate dehydrogenase was diminished for 48 h. Mn2+-superoxide dismutase activity was increased in 30 min, whereas the activity of catalase and glutathione peroxidase remained unaltered. DNA fragmentation and cytochrome c release were maximal in 30 min, but were recovered after 15 h. In conclusion, MEN inhibits intestinal Ca2+ absorption by mitochondrial dysfunction as revealed by GSH depletion and alteration of the permeability triggering the release of cytochrome c and DNA fragmentation. (C) 2007 Elsevier B.V. All rights reserved.
引用
收藏
页码:101 / 107
页数:7
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