Determination of short-chain carboxylic acids and non-targeted analysis of water samples treated by wet air oxidation using gas chromatography-mass spectrometry.

A method based on gas chromatography coupled with electron ionization mass spectrometry employing N,O-bis(trimethylsilyl)trifluoroacetamide with trimethylchlorosilane as derivatization agent was developed to quantify short-chain carboxylic acids (C1-C6) in hospital wastewater treated by wet air oxidation, an advanced oxidation process. Extraction from water and derivatization of volatile and semi-volatile short chain carboxylic acids were optimized and validated and limits of quantification (LOQ = 0.049 mg L-1-4.15 mg L-1), repeatability (RSD = 1.7-12.8%), recovery (31-119%) and trueness (relative bias = -19.0-3.4%) were acceptable. The validated method was successfully applied to monitor the concentration of organic acids formed after wet air oxidation of water samples. Results showed that the method described herein allowed to identify 38% and up to 46% of the final chemical oxygen demand's composition after wet air oxidation of acetaminophen spiked in deionised water and hospital wastewater samples, respectively. The developed method also allowed to perform qualitative non-targeted analysis in hospital wastewater samples after treatment. Results demonstrated that glycerol, methenamine, and benzoic acid were also present in the samples and their presence was confirmed with reference standards.

Resveratrol interferes with AKT activity and triggers apoptosis in human uterine cancer cells.

BACKGROUND: Endometrial cancer is the fourth most prominent cancer among all feminine cancers in the Western world. Resveratrol, a natural anti-oxidant found in red wine emerging as a novel anticancer agent, exerts antiproliferative and pro-apoptotic activity in various cancer cell types, but its effect on uterine cancer cells is poorly understood. At the molecular level, resveratrol has been reported to inhibit cyclooxygenase (COX) expression and/or activity; in endometrial cancer cells, COX-2 is overexpressed and confers cellular resistance to apoptosis. The aim of the present study was to determine if resveratrol could exert anti-proliferative and pro-apoptotic activity over uterine cancer cells upon inhibition of COX-2 expression and/or activity. Six different human uterine cancer cell lines were used as a model (HeLa, Hec-1A, KLE, RL95-2, Ishikawa and EN-1078D). RESULTS AND DISCUSSION: High-dose of resveratrol triggered apoptosis in five out of six uterine cancer cell lines, as judged from Hoechst nuclear staining and effector caspase cleavage. In accordance, uterine cancer cell proliferation was decreased. Resveratrol also reduced cellular levels of the phosphorylated/active form of anti-apoptotic kinase AKT. Endogenous COX-2 protein levels were decreased, concomitant with a decrease in production of COX metabolites PGE2 and PGF2alpha, in each uterine cancer cell line expressing detectable levels of COX-1 and/or COX-2 in presence of resveratrol. Although COX expression was identified as a target of resveratrol in uterine cancer cells, inhibition of COX activity or exogenously added PGE2 did not modulate the effect of resveratrol on cellular proliferation. CONCLUSION: High-dose of resveratrol exerts tumoricidal activity over uterine cancer cells and regulates COX expression. In these cells, resveratrol would not directly target COX activity, but possibly other enzymes involved in prostaglandin synthesis that act downstream of the COXs.