Fluorogenic sensors capable of spatiotemporal detection of labile Fe2+ are highly valuable for the study of iron homeostasis. The labile form contributes to oxidative stress and is linked to various diseases including stroke. A strategy by incorporating a Fe2+-induced selective N-O cleavage of acylated hydroxylamine moiety into fluorophores has been successfully implemented. The first generation Fe2+-selective fluorescent probe has been developed by engineering the functionality into naphthalimide fluorophore with the generation of desired ‘off-on’ signal (Figure 1). The probe can detect endogenous, basal level of labile Fe2+ pools in living cells. Furthermore, the probe enables the revelation of Zn2+-induced Fe2+ flux, observed in stroke and facilely detect the Fe2+ in the brain tissue of a rat undergoing ischemic stroke ischemic site. To further understand the relationship between labile Fe2+, Zn2+ and mitochondrial damage in ischemic stroke, a new mitochondrial targeting rhodamine derived probe is developed by using the similar design principle. The interplay among the elevated level of Fe2+, Zn2+ and ROS tied with ischemia is uncovered by the probe using cellular and animal models. The studies using the probe reveal the positive interplay among the elevated level of Fe2+, Zn2+ and ROS tied with ischemia in OGD/reperfusion model. Figure 1. Fe2+ responsive fluorogenic probe based on Fe2+ induced selective cleavage of N-O bond.

Fluorescence imaging of Fe(II) flux in ischemic stroke

2019 Fall National Meeting

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