| Rank |
Pathway / Axis |
Cancer / Tumor Context |
Normal Tissue Context |
TSF |
Primary Effect |
Notes / Interpretation |
| 1 |
Mitochondrial redox cycling (electron shuttle) |
Redox modulation; NADH oxidation ↑ (context) |
Mitochondrial efficiency ↑ at low doses (reported) |
P, R |
Bioenergetic modulation |
MB can accept electrons from NADH and donate downstream in the ETC; effects are dose-dependent and context-specific. |
| 2 |
OXPHOS vs glycolysis balance |
Shift toward oxidative metabolism reported in some tumor models |
Improved mitochondrial coupling (low dose) |
R |
Metabolic reprogramming |
Sometimes described as “Warburg reversal,” but more accurately a redox/respiratory modulation that varies by system. |
| 3 |
ROS modulation (biphasic) |
ROS ↑ at higher doses; apoptosis ↑ (reported) |
ROS ↓ or stabilized at lower doses |
P, R |
Redox destabilization (dose-dependent) |
Acts antioxidant at low concentrations; can become pro-oxidant as concentration increases. |
| 4 |
Mitochondrial membrane potential (ΔΨm) |
ΔΨm collapse at higher doses (reported) |
Stabilization possible at low doses |
R |
Mitochondrial stress |
High-dose exposure can impair mitochondrial integrity and promote apoptosis. |
| 5 |
Intrinsic apoptosis signaling |
Caspases ↑; apoptosis ↑ (reported in vitro) |
↔ |
G |
Cell death execution |
Generally downstream of ROS and mitochondrial perturbation. |
| 6 |
Photodynamic ROS generation (light-activated) |
ROS ↑↑ when photoactivated |
Localized ROS if illuminated |
P |
Photoactivated cytotoxicity |
Distinct mechanism: MB acts as a photosensitizer under light exposure. |
| 7 |
Glutathione system modulation (GSR / redox enzymes) |
Redox enzyme modulation reported (model-dependent) |
Redox buffering alteration possible |
R |
Redox regulation |
Some reports show interaction with glutathione metabolism; not a dominant universal pathway. |
| 8 |
Blood–brain barrier penetration |
— |
CNS accumulation (high tissue levels) |
P, R |
Pharmacokinetic property |
MB crosses the BBB and can accumulate in brain tissue at higher concentrations than plasma. |
| 9 |
Monoamine oxidase (MAO) inhibition |
— |
MAO-A inhibition (clinically relevant) |
R |
Off-target pharmacology |
Important interaction risk with SSRIs/SNRIs (serotonin syndrome). |
| 10 |
Safety constraints (G6PD deficiency; serotonin syndrome) |
— |
Hemolysis risk (G6PD); serotonin toxicity risk |
— |
Clinical risk management |
Well-established safety considerations in clinical use. |