Simultaneous detection of mitochondrial viscosity and peroxynitrite in livers from subjects with drug-induced fatty liver disease using a novel fluorescent probe

Drug-induced fatty liver disease (DIFLD) is a basic clinicopathological example of drug-induced liver injury (DILI). Some drugs can inhibit β-oxidation in hepatocyte mitochondria, leading to steatosis in the liver. Additionally, drug-induced inhibition of β-oxidation and the electron transport chain...

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Published inTalanta (Oxford) Vol. 260; p. 124591
Main Authors Niu, Linqiang, Cao, Qijuan, Zhang, Tian, Zhang, Yahong, Liang, Tingting, Wang, Jianhong
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier B.V 01.08.2023
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Summary:Drug-induced fatty liver disease (DIFLD) is a basic clinicopathological example of drug-induced liver injury (DILI). Some drugs can inhibit β-oxidation in hepatocyte mitochondria, leading to steatosis in the liver. Additionally, drug-induced inhibition of β-oxidation and the electron transport chain (ETC) can lead to increased production of reactive oxygen species (ROS) such as peroxynitrite (ONOO−). Therefore, it is reasonable to suspect that compared to a healthy liver, viscosity and ONOO− levels are elevated in livers during DIFLD. A novel, smart, dual-response fluorescent probe—Mito-VO—was designed and synthesized for the simultaneous detection of viscosity and ONOO− content. This probe had a large emission shift of 293 nm and was capable of monitoring the viscosity of, and the ONOO− content in, cell and animal models alike, either individually or simultaneously. For the first time, Mito-VO was successfully used to demonstrate the elevated viscosity and the amount of ONOO− in livers from mice with DIFLD. [Display omitted] •A dual-response fluorescent probe could simultaneously detect viscosity and ONOO−.•The probe had a large emission shift of 293 nm.•The probe was capable of monitoring cell and animal models alike.•The probe was used to detect viscosity and ONOO− in livers from mice with DIFLD.
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ISSN:0039-9140
1873-3573
1873-3573
DOI:10.1016/j.talanta.2023.124591