The Claim
Hydrazine, a metabolite of isoniazid, inhibits mitochondrial complex II activity in mouse liver mitochondria with an IC50 of approximately 30 μM, and the formation of hydrazine is necessary for the synergistic hepatotoxicity of efavirenz and isoniazid, as inhibition of hydrazine production by bis-p-nitrophenyl phosphate prevents cell death.
What the research says
Supports is higher
Support is ahead, but a single strong opposing study can change this.
These are independent scores, not a percentage. Higher-grade studies count more, so a single strong opposing study can outweigh several weaker ones.
A chemical called hydrazine, which the body makes when it breaks down a tuberculosis drug, can damage liver cells by disrupting energy production in mitochondria. When combined with another drug (efavirenz), this damage gets worse—but if you stop hydrazine from forming, the liver cells don’t die.
See the scientific wording
Hydrazine, a metabolite of isoniazid, inhibits mitochondrial complex II activity in mouse liver mitochondria with an IC50 of approximately 30 μM, and its formation is necessary for the synergistic hepatotoxicity of efavirenz and isoniazid, as blocking its production with bis-p-nitrophenyl phosphate prevents cell death.
What the research says
1 studyWhen taken together, two drugs (isoniazid and efavirenz) can hurt the liver because one of them turns into a harmful substance called hydrazine that breaks down energy production in liver cells. Stopping hydrazine from forming stops the damage.
Score breakdown, mechanism chain, raw evidence, ideal studies needed & 1 supporting studies
Not medical advice. For informational purposes only. Always consult a qualified healthcare professional before making health decisions.