Keap1-nrf2 signaling: a target for cancer prevention by sulforaphane.
Level 5 - mechanism / opinion, no new human data
Narrative review of mechanisms and previously conducted clinical studies
PubMed 22752583 · doi:10.1007/128_2012_339
What was done
This narrative review summarizes preclinical mechanisms of sulforaphane targeting the Keap1-Nrf2 stress-response pathway and describes a series of clinical trials conducted in Qidong, China. Those trials evaluated broccoli sprout beverages containing glucoraphanin and sulforaphane for bioavailability, tolerability, and pharmacodynamic effects against environmental carcinogen exposures.
What was found
The abstract presents no quantitative data or statistical values. It reports qualitatively that sulforaphane prevents Keap1-mediated degradation of Nrf2, promoting nuclear accumulation and transcription of cytoprotective genes. In human trials, broccoli sprout preparations enhanced the detoxification of aflatoxins and airborne toxins.
Why it matters
It details how dietary phytochemicals from broccoli sprouts can activate the Keap1-Nrf2 pathway to enhance chemical clearance in populations exposed to environmental toxins.
Limits
The abstract contains no sample sizes, effect sizes, or quantitative data. As a narrative review, it lacks systematic search methodology, and long-term reduction in clinical cancer incidence was not established.
Cited by
- supports Sulforaphane activates the antioxidant response element by binding or interacting with Keap1 in the cytoplasm, triggering the release and nuclear translocation of Nrf2.