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. 2019 Aug 21;8(9):327. doi: 10.3390/antiox8090327

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Induction of mitochondrial dysfunction by genistein in T24 cells. The cells were cultured for 48 h in media containing different concentrations of genistein. (A,B) The levels of mRNA and protein of Bcl-2 family members were examined by RT-PCR and Western blot analysis. (C,D) The effect of genistein on mitochondrial membrane potential (MMP) was analyzed by a flow cytometer (*** p < 0.0001, when compared to control). (E) Cytoplasmic and mitochondrial proteins were isolated for analysis of cytochrome c expression, and Western blot analysis was performed. Analysis of cytochrome oxidase subunit VI (COX VI) and actin expression was performed to confirm the protein loading of each fraction extract.

Induction of mitochondrial dysfunction by genistein in T24 cells. The cells were cultured for 48 h in media containing different concentrations of genistein. (A,B) The levels of mRNA and protein of Bcl-2 family members were examined by RT-PCR and Western blot analysis. (C,D) The effect of genistein on mitochondrial membrane potential (MMP) was analyzed by a flow cytometer (*** p < 0.0001, when compared to control). (E) Cytoplasmic and mitochondrial proteins were isolated for analysis of cytochrome c expression, and Western blot analysis was performed. Analysis of cytochrome oxidase subunit VI (COX VI) and actin expression was performed to confirm the protein loading of each fraction extract.