摘要
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 ‘offon’ signal(Fig.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.