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| Reverse Electron Transport (RET) — Mitochondrial electron-transport process in which electrons flow in the reverse direction from a highly reduced coenzyme Q (ubiquinol; QH2) pool through respiratory Complex I toward NAD+, rather than through the normal forward electron-transfer pathway. RET is favored by a high mitochondrial membrane potential and strongly reduced CoQ pool and can generate substantial mitochondrial superoxide/ROS at Complex I. Typical modulation in cancer: Context-dependent. Increased RET can elevate mitochondrial ROS and promote oxidative stress, signaling, or cell death, but tumor cells may also exploit RET-derived ROS as signaling molecules under selected metabolic conditions. A universal anticancer direction should therefore not be assigned. Typical mechanistic relationship: High mitochondrial membrane potential + highly reduced CoQ pool → RET ↑ → Complex I superoxide / mtROS ↑. |
| 8658- | MLT, | Melatonin drives apoptosis in head and neck cancer by increasing mitochondrial ROS generated via reverse electron transport |
| - | vitro+vivo, | SCC, | CAL27 | - | in-vitro, | Tong, | SCC9 |
Query results interpretion may depend on "conditions" listed in the research papers. Such Conditions may include : -low or high Dose -format for product, such as nano of lipid formations -different cell line effects -synergies with other products -if effect was for normal or cancerous cells
Filter Conditions: Pro/AntiFlg:% IllCat:% CanType:% Cells:0 prod#:% Target#:1882 State#:% Dir#:2
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