Epidemiological evidences establish sulforaphane (SFN), a hormetic dietary isothiocyanate to be a promising
chemopreventive, anti-inflammatory and anti-cancer agent. Beyond a concentration threshold SFN exerts pro-death
activities (cell cycle arrest, epigenetic modifications and apoptosis) and below the threshold it either promotes prosurvival
autophagy or remains latent. There is a significant lacuna in understanding the underpinning dynamic molecular
networks that alternate the pharmacological responses with respect to the intracellular concentration and exposure time
that renders SFN to be a characteristic hormetic molecule (display characteristic biphasic dose response curve).
Unraveling this multi-targeted SFN triggered molecular interplay between apoptosis and pro-survival autophagy may have
great therapeutic implications. From the available literature, here we present a review that illustrates the existence of a
hormetic window and briefly discussed its role in the spectrum of activity of SFN in different pathological conditions
(cancer and immune-mediated diseases). Further, we hypothesize a hormetic signaling event on how SFN triggers
mutually exclusive molecular pathways such as cell survival or death signals depending on its pathophysiological
environment, exposure time and in vitro working concentrations. By better understanding these altered events and
underpinning mechanisms in different combinations such as concentrations and time a proper therapeutic can be designed.
Keywords: Apoptosis, autophagy, hormesis, isothiocyanates, phytochemicals, sulforaphane.
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