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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

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

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

Exogenous H2S initiating Nrf2/GPx4/GSH pathway through promoting Syvn1-Keap1 interaction in diabetic hearts

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