Taking 120 micromoles of sulforaphane daily for a year does not change levels of Caspase-3 or TUNEL markers in the bronchial tissue of former smokers.
Mechanism
Synthesis from 1 study
Sulforaphane turns on a cellular cleanup system that removes harmful chemicals from smoking. This stops lung cells from dividing too quickly, but it does not make them die. The cells just stop multiplying.
Most probable mechanism
Sulforaphane enters lung cells and turns on a protective system that cleans up harmful chemicals from smoking. This reduces damage to DNA, which stops the cells from dividing too fast. The cells do not die off more than usual; they just stop multiplying.
Sulforaphane is absorbed from the gut and reaches bronchial epithelial cells in the airways
Sulforaphane modifies specific cysteine residues on the Keap1 protein, preventing it from tagging Nrf2 for degradation
Stabilized Nrf2 translocates to the nucleus and binds to antioxidant response elements, increasing transcription of detoxification and cytoprotective genes
Enhanced detoxification reduces oxidative DNA damage in bronchial epithelial cells
Reduced DNA damage decreases signaling that drives cell cycle progression, leading to lower Ki-67 expression and suppressed proliferation
Caspase-3 activation and DNA fragmentation measured by TUNEL remain unchanged, indicating no increase in apoptotic cell death
Evidence from Studies
Supporting (1)
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Contradicting (0)
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