Biochar activation methods have attracted extensive attention due to their great role in improving sorptive properties of carbon-based materials. As a result, chemically modified biochars gained application potential in the purification of soil and water from xenobiotics. This paper describes changes in selected physicochemical properties of high-temperature wheat-straw biochar (BC) upon its deashing. On the pristine and chemically activated biochar (BCd) retention of five pesticides of endocrine disrupting activity (carbaryl, carbofuran, 2,4-D, MCPA and metolachlor) was studied. Deashing resulted in increased sorbent aromaticity and abundance in surface hydroxyl groups. BCd exhibited more developed meso- and microporosity and nearly triple the surface area of BC. Hydrophobic pesticides (metolachlor and carbamates) displayed comparably high (88–98%) and irreversible adsorption on both BCs, due to the pore filling, whereas the hydrophilic and ionic phenoxyacetic acids were weakly and reversibly sorbed on BC (7.3 and 39% of 2,4-D and MCPA dose introduced). Their removal from solution and hence retention on the deashed biochar was nearly total, due to the increased sorbent surface area and interactions of the agrochemicals with unclogged OH groups. The modified biochar has the potential to serve as a superabsorbent, immobilizing organic pollutant of diverse hydrophobicity from water and soil solution.

Quantification with satisfactory specificity and sensitivity of free 3-Nitro-l-tyrosine (3-NT), 3-Chloro-l-tyrosine (3-CT), and 3-Bromo-l-tyrosine (3-BT) in biological samples as potential inflammation, oxidative stress, and cancer biomarkers is analytically challenging. We aimed at developing a liquid chromatography–tandem mass spectrometry (LC-MS/MS)-based method for their simultaneous analysis without an extract purification step by solid-phase extraction. Validation of the developed method yielded the following limits of detection (LOD) and quantification (LOQ) for 3-NT, 3-BT, and 3-CT: 0.030, 0.026, 0.030 ng/mL (LODs) and 0.100, 0.096, 0.098 ng/mL (LOQs). Coefficients of variation for all metabolites and tested concentrations were <10% and accuracy was within 95–105%. Method applicability was tested on colorectal cancer patients during the perioperative period. All metabolites were significantly higher in cancer patients than healthy controls. The 3-NT was significantly lower in advanced cancer and 3-BT showed a similar tendency. Dynamics of 3-BT in the early postoperative period were affected by type of surgery and presence of surgical site infections. In conclusion, a sensitive and specific LC-MS/MS method for simultaneous quantification of free 3-NT, 3-BT, and 3-CT in human plasma has been developed.

Molecular mechanisms underlying the beneficial effect of sitagliptin repurposed for hepatic ischemia-reperfusion injury (IRI) are poorly understood. We aimed to evaluate the impact of IRI and sitagliptin on the hepatic profile of eicosanoids (LC-MS/MS) and expression/concentration (RTqPCR/ELISA) of GLP-1/GLP-1R, SDF-1α/CXCR4 and VIP/VPAC1, VPAC2, and PAC1 in 36 rats. Animals were divided into four groups and subjected to ischemia (60 min) and reperfusion (24 h) with or without pretreatment with sitagliptin (5 mg/kg) (IR and SIR) or sham-operated with or without sitagliptin pretreatment (controls and sitagliptin). PGI₂, PGE₂, and 13,14-dihydro-PGE₁ were significantly upregulated in IR but not SIR, while sitagliptin upregulated PGD₂ and 15-deoxy-12,14-PGJ₂. IR and sitagliptin non-significantly upregulated GLP-1 while Glp1r expression was borderline detectable. VIP concentration and Vpac2 expression were downregulated in IR but not SIR, while Vpac1 was significantly downregulated solely in SIR. IRI upregulated both CXCR4 expression and concentration, and sitagliptin pretreatment abrogated receptor overexpression and downregulated Sdf1. In conclusion, hepatic IRI is accompanied by an elevation in proinflammatory prostanoids and overexpression of CXCR4, combined with downregulation of VIP/VPAC2. Beneficial effects of sitagliptin during hepatic IRI might be mediated by drug-induced normalization of proinflammatory prostanoids and upregulation of PGD₂ and by concomitant downregulation of SDF-1α/CXCR4 and reinstating VIP/VCAP2 signaling.