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To elucidate the complex role of biological H2S and study the mitochondrial damage and some related diseases, effective methods for visualization of H2S in mitochondria and in vivo are urgently needed. In this contribution, a novel near-infrared mitochondria-targetable fluorescence probe MI-H2S for H2S detection was developed. MI-H2S shows rapid detection ability for H2S in pure aqueous solution and outputs a highly selective and sensitive fluorescence-on signal at 663 nm with a large Stokes shift of 141 nm. Bioimaging experiments revealed that the probe has good mitochondrial-targeting ability and high-contrast imaging ability for detecting H2S in living systems. The probe also showed great potential in the detection of H2S during inflammation. All of the results demonstrate that MI-H2S can be applied as an effective probe for the visualization and study of H2S in mitochondria and in vivo.

To elucidate the complex role of biological H

Both glutathione (GSH) and viscosity play an important role in mitochondria. They are closely related to various physiological and pathological processes and are important biomarkers in cancer analysis. Herein, we developed the first dual responsive fluorescence probe MGV that can simultaneously detect mitochondrial GSH and viscosity. MGV is smart and shows a selective ratiometric response to GSH at 535/650 nm with a significant increase of green fluorescence. MGV can also show a distinct red fluorescence enhancement at 627 nm as viscosity increases. In addition, MGV has low cytotoxicity and good mitochondrial-targeting ability. With these features, MGV was successfully applied to image mitochondrial GSH at dual fluorescence channels and track mitochondrial viscosity changes on the red fluorescence channel. With MGV, the formation of mitochondrial bleb vesicles was observed with nystatin stimulation, and during the Cisplatin-induced apoptosis, both the level of GSH and the viscosity showed an increase. Finally, based on the dual-response to GSH and viscosity, MGV was successfully used for dual-channel imaging of cancer cells/tumors. Overall, this work provided a smart probe for GSH and viscosity and new insights/methods for apoptosis and tumor imaging.

Carbon monoxide (CO) plays a vital role in living organisms. The detection of CO at the subcellular level is of great significance to clarify its biological functions. Increasing evidence shows that CO is important in Golgi apparatus, but so far, no probe has been reported to detect CO in Golgi. In this paper, an effective fluorescence probe Gol-CO was reported for CO imaging in Golgi apparatus. Gol-CO uses a Golgi-targetable aminoquinoline derivative as the fluorophore and importantly, it shows significant ratiometric fluorescence signal changes at 520/425 nm in aqueous solutions with high selectivity and sensitivity (about 41 nM of detection limit) for CO. Imaging experiments showed that Gol-CO has excellent targeting ability to Golgi apparatus and excellent ratiometric fluorescence imaging ability for CO in cells and zebrafish. Gol-CO also succeeded in visualizing the level increase of CO in living cells under oxidative stress.

Previous studies have reported that female gender confers cardioprotection against ischemia/reperfusion (I/R) injury, partly because estrogen activates phosphatidylinositol-3-kinase/Akt (PI3K/Akt) pathway. We have previously proven that cardioprotection of sevoflurane postconditioning is mediated by PI3K/Akt pathway in male rats. The purpose of the present study was to determine whether the cardioprotection of sevoflurane postconditioning is influenced by gender, and the role of PI3K/Akt pathway in such gender difference.Isolated hearts from 2-mo-old male and female SD rats were subjected to ischemia for 40 min and reperfusion for 2 h in the Langendorff apparatus, and were randomly assigned to the following groups: no ischemia/reperfusion (CON), ischemia/reperfusion (I/R), I/R+sevoflurane postconditioning (I/R+SPC), I/R+100 nM wortmannin (I/R+WOR), and I/R+SPC+WOR. Postconditioning was performed with administration of 3.0% sevoflurane at the first 10 min of reperfusion. Left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), and myocardial lactate dehydrogenase (LDH) release were measured. Infarct size was detected by riphenyltetrazolium chloride staining. The protein expression of total Akt (t-Akt) and phosphorylated Akt (Ser(473)) (p-Akt) were determined by Western blot.The I/R group showed lower LVDP and higher LVEDP than CON group in the same gender during reperfusion period. The LDH release and infarct size were smaller in the female I/R group (P0.05 versus male I/R group). Sevoflurane postconditioning markedly improved left ventricular function and decreased LDH, infarct size in the male I/R+SPC group (P0.05 versus male I/R group) but not in the female I/R+SPC group. Wortmannin abolished the cardioprotection of sevoflurane postconditioning in the male I/R+SPC+Wort group (P0.05 versus male I/R+SPC group), and markedly increased the infarct size and LVEDP and decreased LVDP in female rats. The t-Akt protein expression was no significant difference in all groups. The ratio of p-Akt/t-Akt expression in the male CON group was a little lower than that in the female CON group, but there was no statistical significance. In male rats, the ratio of p-Akt/t-Akt was no difference between CON and I/R group, but it was higher in I/R+SPC group than that in I/R group (P0.05). In female rats, the level of p-Akt was markedly increased by I/R, which was markedly higher than that in male I/R group (P0.05). However, p-Akt was not different between I/R and I/R+SPC groups. Wortmannin decreased the p-Akt expression in both male and female rats.It is concluded that female rat hearts showed greater resistance to I/R injury, and sevoflurane postconditioning developed cardioprotection in male rats but not in female rats. The PI3K/Akt pathway may be involved in the cardioprotection by both sevoflurane postconditioning and gender.