Methylene blue can help mitochondria keep working when the first part of their energy system is broken, but it doesn't work at all when the second part is broken.
Scientific Claim
In mouse brain mitochondria oxidizing NADH-generating substrates, methylene blue (1 μM) restores mitochondrial membrane potential and respiration inhibited by rotenone (Complex I blockade), but fails to restore membrane potential or respiration inhibited by antimycin (Complex III blockade), indicating its electron-shuttling activity is dependent on an intact Complex III.
Original Statement
“We found that in mouse brain mitochondria, MB fails to restore the membrane potential and respiration inhibited by antimycin... MB could act as an alternative electron acceptor bypassing Complex I inhibition... MB did not restore the ΔΨm in the mitochondria oxidizing either pyruvate + malate, succinate, or L-proline.”
Evidence Quality Assessment
Claim Status
appropriately stated
Study Design Support
Design supports claim
Appropriate Language Strength
definitive
Can make definitive causal claims
Assessment Explanation
The study used direct, controlled measurements of mitochondrial function in isolated tissue under defined inhibitor conditions. The results are consistent, reproducible (n=8 for ΔΨm), and directly test the mechanism. Definitive language is appropriate for the observed in vitro effects.
Evidence from Studies
Supporting (1)
Methylene blue does not bypass Complex III antimycin block in mouse brain mitochondria
Methylene blue can help fix broken energy production in mitochondria when the first part (Complex I) is broken, but it can't fix it when the second part (Complex III) is broken—because it needs Complex III to work.