L-cystine-linked BODIPY-adsorbed monolayer MoS2 quantum dots for ratiometric fluorescent sensing of biothiols based on the inner filter effect

Abstract

This study fabricated a dual-emission probe consisting of monolayer MoS2 quantum dots (M − MoS2 QDs) and L-cystine-linked boron-dipyrromethene (L-Cys-BODIPY) molecules for ratiometric sensing of biothiols, thiol product-related enzyme reactions, and ratiometric imaging of glutathione (GSH)-related reactions in HeLa cells. The formation of L-Cys-BODIPY-adsorbed M − MoS2 QDs (named as BODIPY-M-MoS2 QDs) was demonstrated by comparing them with M − MoS2 QDs using transmission electron microscopy, atomic force microscopy, and X-ray photoelectron spectroscopy. The BODIPY-M-MoS2 QDs exhibited dual-emission bands, excellent biocompatibility, and good resistance to photobleaching. It was found that the adsorbed L-Cys-BODIPY molecules rarely quenched the fluorescence of M − MoS2 QDs, and meanwhile, they were self-quenched by π-π stacking between each BODIPY backbones. The presence of biothiols induced the reduction of weakly fluorescent L-Cys-BODIPY to strongly fluorescent of L-cysteine-conjugated BODIPY. Since having a much higher molar absorption coefficient than L-Cys-BODIPY, the liberated L-cysteine-conjugated BODIPY behaved as an effective inner filter to absorb the excitation light and subsequently quenched the fluorescence of M − MoS2 QDs. The appearance of L-cysteine-conjugated BODIPY could barely affected to the fluorescence lifetime of M − MoS2 QDs, confirming the inner filter effect of L-cysteine-conjugated BODIPY onto the fluorescence of M − MoS2 QDs. The present probe not only provided a linear ratiometric response to 1–10 mM GSH, 1–10 μM cysteine, and 1–10 μM of homocysteine but also remarkably showed the ratiometric detection of thiol products from the reactions of 1–900 units L−1 S-adenosylhomocysteine (SAH) hydrolase and SAH as well as 1–850 units L−1 GSH reductase and disulfide GSH. Additionally, the present probe was well-suited for ratiometric imaging of intracellular GSH levels in non-treated and drug-treated HeLa cells.