Mitochondrial alterations induced by aspirin in rat hepatocytes expressing mitochondrially targeted green fluorescent protein (mtGFP)

FEBS Letters

Rizzuto, R.¹  Venerando, R.²  Miotto, G.²  Siliprandi, N.²  Pizzo, P.¹ 

[1] Department of Biomedical Sciences, University of Padova, Via Trieste, 75, 35121 Padova, Italy;Department of Biological Chemistry, CNR Center for the Study of Mitochondrial Physiology, University of Padova, Via Trieste, 75, 35121 Padova, Italy

关键词: Acetylsalicylate;    Cyclosporin A;    GFP;    Hepatocyte;    Rat liver mitochondria;    ASA;    acetylsalicylate;    CsA;    cyclosporin;    MPT;    membrane permeability transition;    mtGFP;    mitochondrially targeted green fluorescent protein;   

DOI  :  10.1016/0014-5793(96)00182-2

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

Mitochondria in primary living hepatocytes were visualized in cells transfected with a chimeric plasmid encoding for the green fluorescent protein (GFP) of Aequorea victoria engineered to be specifically targeted to mitochondria, as described recently (Rizzuto et al. (1995) Curr. Biol. 5, 635–642). The identification of the fluorescent organelles as authentic mitochondria was confirmed by double labeling with rhodamine 123. Acetylsalicylate treatment of hepatocytes induced in mitochondria typical morphological alterations closely analogous to the swelling promoted by acetylsalicylate in isolated mitochondria. Cyclosporin A, which in isolated mitochondria prevents the changes induced by acetylsalicylate, had no protective action but induced per se specific alterations in the morphology of mitochondria. Moreover, exposure of hepatocytes to cyclosporin A followed by acetylsalicylate caused the same mitochondrial changes induced by each of the two compounds separately. The structural alterations caused by acetylsalicylate were constantly associated with a decrease in mitochondrial urea synthesis and cell viability.

【 授权许可】

Unknown