Amavadin induced PTP opening not through the promotion of ROS generation in rat kidney mitochondria

doi:10.5246/jcps.2014.12.105

Abstract

Abstract:

Amavadin is a natural vanadium compound that accumulates to high level in poisonous Amanita mushrooms. Recently, amavadin was found to have potential therapeutic effect in cancer treatment. However, its toxicity and the possible mechanism of actions are still not clear. In this study, we investigated the toxic effects of amavadin on rat kidney mitochondriaand the possible mechanism. We found that amavadin induced significantly permeability transition pore (PTP) opening in the mitochondria. Amavadin concentration-dependently inhibited the generation of reactiveoxygen species (ROS) in succinate buffer, and at high concentration of 200 μM it increased the ROS generation in malate buffer. With the addition of rotenone, the ROS generation in malate buffer was strongly enhanced than that induced by amavadin alone, but remained unchanged in succinate buffer. Results from the present study suggest that amavadin act upon electron transport chain downstream of rotenone, and the ubiquinone binding site in complex I is the most possible binding site.

Key words: Amavadin, Vanadium compound, Mitochondria, Reactive oxygen species, Permeability transition pore

CLC Number:

R915

Supporting:

Chenyi Huo, Huixue Liu. Amavadin induced PTP opening not through the promotion of ROS generation in rat kidney mitochondria[J]. Journal of Chinese Pharmaceutical Sciences, 2014, 23(12): 830-836.

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