Switchable aptamer-fueled colorimetric sensing toward agricultural fipronil exposure sensitized with affiliative metal-organic framework.

Persistent usage of pesticides in agriculture has posed serious damage to overall ecosystem and human health, and thereby it is imperative to develop sensitive and efficient tools to evaluate residual pesticides in food and environmental setting. Herein, we reported a switchable colorimetric probe toward fipronil residue sensitized with aptamer-fueled catalytic activity of affiliative ZIF-8. Innovatively, it was found that the attached aptamer preferred to adsorb 3,3',5,5'-tetramethylbenzidine (TMB) rather than 2,2-azinobis (3-ethylbenzothiazo-line-6-sulfonic acid) (ABTS), greatly promoting catalytic oxidation of ZIF-8 toward TMB for further improving sensitivity. Aiding with smartphone-based image acquisition, fipronil-responsive discoloration degree was converted into the ratio of green and blue (G/B) with limit of detection as low as 0.036 µM (0.016 µg·g-1). Moreover, it allowed for fipronil analysis in water, soil and vegetable samples with good recovery between 87 % and 110 %, verifying extension application prospect of the aptamer-fueled colorimetry for on-field pesticide evaluation in food safety supervision.

Development and validation of the UPLC-MS method for simultaneous determination of six new psychoactive substances.

The combined abuse of benzodiazepines and antipsychotics has become a global problem, and to develop a highly sensitive and selective method for monitoring of benzodiazepine hypnotics and antipsychotics is urgently necessary. In this work, we established a rapid method for the simultaneous determination of benzodiazepines (diazepam, alprazolam, triazolam, and estazolam) and antipsychotic drugs (clozapine, and chlorpromazine) based on ultra performance liquid chromatography-mass spectrometry (UPLC-MS). The accuracy, precision, limit of detection (LOD), limit of quantification (LOQ), specificity, matrix effect and carry-over effect were verified in detail. The results of the recovery and repeat experiments proved that the proposed UPLC-MS method possessed very satisfactory accuracy and precision. The LOD and LOQ of the six psychoactive substances were as low as 0.001-0.005 and 0.005-0.01 µg L-1, respectively. The proposed method was employed to analyze urine samples which were pretreated with a protein precipitation process. The potential influences of precipitants on the analysis results were evaluated statistically, and 0.1% formic acid/acetonitrile/water was selected as the optimum precipitation agent. The detection of the targets was free from matrix and carryover effects.

Thioredoxin-1 blocks methamphetamine-induced injury in brain through inhibiting endoplasmic reticulum and mitochondria-mediated apoptosis in mice.

Methamphetamine (METH) has been reported to induce endoplasmic reticulum (ER) stress and neuronal apoptosis in the central nervous system (CNS) during the development of addiction. Thioredoxin-1 (Trx-1) is a redox regulating protein and plays an important role in inhibiting apoptosis and protects neurons from cytotoxicity through ER and mitochondria-mediated pathways. Our previous study has been reported that Trx-1 protects mice from METH-induced rewarding effect. However, whether Trx-1 plays the role in resisting METH injury is still unclear. Here, we aim to investigate whether Trx-1 participates in the regulation of METH-induced CNS injury via ER stress and mitochondria-mediated pathways. Our study first repeated the conditioned place preference expression induced by METH. Then we detected and found that METH increased the expression of N-methyl-d-asparate (NMDA) receptor subunit 2B (NR2B) and the level of glutamate (Glu) in the ventral tegmental area (VTA) and nucleus accumbens (NAc), while Trx-1 overexpression suppressed the increases. We further examined ER stress-related proteins and mitochondrial apoptosis pathway in the VTA and NAc, and found that METH increased the expressions of glucose regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), and Bax, as same time decreased the expressions of procaspase12, Bcl-2, and procaspase3, while Trx-1 overexpression blocked these changes. These results indicate that Trx-1 blocks METH-induced injury by suppressing ER stress and mitochondria-mediated apoptosis in the VTA and NAc via targeting glutamatergic system.