NDLI: Water-soluble formulation of Coenzyme Q10 inhibits Bax-induced destabilization of mitochondria in mammalian cells

Content Provider	Springer Nature Link
Author	Naderi, Jafar Somayajulu Nitu, Mallika Mukerji, Amit Sharda, Priya Sikorska, Marianna Borowy Borowski, Henryk Antonsson, Bru Pandey, Siyaram
Copyright Year	2006
Abstract	Oxidative stress leads to mitochondrial dysfunction, which triggers the opening of the permeability transition pores (PTP) and the release of pro-apoptotic factors causing apoptotic cell death. In a limited number of cell systems, anti-oxidants and free-radical scavengers have been shown to block this response. We have previously reported that coenzyme Q10 (CoQ10), an electron carrier in the mitochondrial respiratory chain, is involved in the reactive oxygen species (ROS) removal and prevention of oxidative stress-induced apoptosis in neuronal cells. However, the mechanism of this protection has not been fully elucidated. In the present study we investigated the effects of CoQ10 on the mitochondrial events characteristic to apoptosis, especially on the function of pro-apoptotic protein Bax. Our results demonstrated that following a brief exposure of two human cell lines (fibroblasts and HEK293 cells) to H2O2 the intracellular levels of ROS and the association of Bax with the mitochondria significantly increased and the cells underwent apoptosis. Both of these events, as well as the release of cytochrome c from the mitochondria, were blocked by a 24 h pre-treatment with CoQ10. It is therefore believed that CoQ10 prevented the collapse of the mitochondrial membrane potential in response to the H2O2 treatment. Recombinant Bax protein alone caused the ROS generation and release of cytochrome c from isolated mitochondria and, again, CoQ10 inhibited these Bax-induced mitochondrial dysfunctions.
Starting Page	1359
Ending Page	1369
Page Count	11
File Format	PDF
ISSN	13608185
Journal	Apoptosis
Volume Number	11
Issue Number	8
e-ISSN	1573675X
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2006-05-30
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Apoptosis Bax CoQ10 Mitochondrial dysfunction Oxidative stress Permeability transition pores Cancer Research Virology Oncology Biochemistry Cell Biology
Content Type	Text
Resource Type	Article
Subject	Pharmaceutical Science Biochemistry (medical) Cell Biology Clinical Biochemistry Cancer Research Pharmacology

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