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Nickel AG, Von Hardenberg A, Hohl M, Lffler JR, Kohlhaas M, Becker J, Reil JC, Kazakov A, Bonnekoh J, Stadelmaier M, Puhl SL, Wagner M, Bogeski I, Cortassa S, Kappl R, Pasieka B, Lafontaine M, Lancaster CRD, Blacker TS, Hall AR, Duchen MR, Kstner L, Lipp P, Zeller T, Mller C, Knopp A, Laufs U, Bhm M, Hoth M, Maack C (2015) Reversal of mitochondrial transhydrogenase causes oxidative stress in heart failure

doi:10.1097/00129492-200301000-00023 Lampert L, Wong YJ

However, there remains a lack of systematic reviews detailing the molecular mechanisms by which ginsenosides reduce blood lipid levels, especially in relation to oxidative stress

We next investigated whether mitochondria are the source of ROS generation in RPE cells upon GSH depletion, we used MitoSOX Red to detect mitochondrial ROS (Fig