Dispersive liquid–liquid microextraction of 11-nor-Δ9-tetrahydrocannabinol-carboxylic acid applied to urine testing

Aim: THC-COOH is the major metabolite of Δ9-tetrahydrocannabinol commonly tested in urine to determine cannabis intake. In this study, a method based on dispersive liquid–liquid microextraction was developed for testing THC-COOH in urine. Materials & methods: Hydrolyzed urine specimens were extracted via dispersive liquid–liquid microextraction with acetonitrile (disperser solvent) and chloroform (extraction solvent). Derivatization was performed with N,O-Bis(trimethylsilyl)trifluoroacetamide with 1% trichloro(chloromethyl)silane. Analysis was performed by GC–MS/MS. Results: The method showed acceptable linearity (5–500 ng/ml), imprecision (<10.5%) and bias (<4.9%). Limits of detection and quantitation were 1 and 5 ng/ml, respectively. Twenty-four authentic samples were analyzed, with 22 samples being positive for THC-COOH. Conclusion: The proposed method is more environmentally friendly and provided good sensitivity, selectivity and reproducibility.

Effects of Glyphosate and Its Metabolite AMPA on Aquatic Organisms

Glyphosate (N-(phosphonomethyl)glycine) was developed in the early 1970s and at present is used as a herbicide to kill broadleaf weeds and grass. The widely occurring degradation product aminomethylphosphonic acid (AMPA) is a result of glyphosate and amino-polyphosphonate degradation. The massive use of the parent compound leads to the ubiquity of AMPA in the environment, and particularly in water. Considering this, it can be assumed that glyphosate and its major metabolites could pose a potential risk to aquatic organisms. This review summarizes current knowledge about residual glyphosate and its major metabolite AMPA in the aquatic environment, including its status and toxic effects in aquatic organisms, mainly fish. Based on the above, we identify major gaps in the current knowledge and some directions for future research knowledge about the effects of worldwide use of herbicide glyphosate and its major metabolite AMPA. The toxic effect of glyphosate and its major metabolite AMPA has mainly influenced growth, early development, oxidative stress biomarkers, antioxidant enzymes, haematological, and biochemical plasma indices and also caused histopathological changes in aquatic organisms.

Effects of Glyphosate and Their Metabolite AMPA on Aquatic Organisms

Glyphosate (N-(phosphonomethyl)glycine) is a herbicide used to kill broadleaf weeds and grass, developed in the early 1970s. The widely occurring degradation product aminomethylphosphonic acid (AMPA) is a result of glyphosate and amino-polyphosphonate degradation. The massive use of the parent compounds leads to the ubiquity of AMPA in the environment, and particularly in water. Considering this, it can be assumed that glyphosate and its major metabolites could pose a potential risk to aquatic organisms. This review summarises current knowledge about residual glyphosate and their major metabolite AMPA in the aquatic environment, including status and toxic effects in aquatic organisms, mainly fish, are reviewed. Based on the above, we identify major gaps in the current knowledge and some directions for future research knowledge about the effects of worldwide use of herbicide glyphosate and its major metabolite AMPA. The toxic effect of glyphosate and their major metabolite AMPA has mainly influenced growth, early development, oxidative stress biomarkers, antioxidant enzymes, haematological, biochemical plasma indices, caused histopathological changes in the aquatic organism.

NNAL, a major metabolite of tobacco-specific carcinogen NNK, promotes lung cancer progression through deactivating LKB1 in an isomer-dependent manner

Smoking is associated with worse clinical outcomes for lung cancer patients. Cell-based studies suggest that NNK (a tobacco specific carcinogen) promotes lung cancer progression. Given its short half-life, the physiological relevance of these in vitro results remains elusive. NNAL, a major metabolite of NNK with a similar structure, a chiral center, and a longer half-life, has never been evaluated in cancer cells. In this study, we characterized the effect of NNAL and its enantiomers on cancer progression among a panel of NSCLC cell lines and explored the associated mechanisms. We found that (R)-NNAL promotes cell proliferation, enhances migration, and induces drug resistance while (S)-NNAL has much weaker effects. Mechanistically, (R)-NNAL phosphorylates and deactivates LKB1 via the β-AR signaling in the LKB1 wild type NSCLC cell lines, contributing to the enhanced proliferation, migration, and drug resistance. Of note, NNK exposure also increases the phosphorylation of LKB1 in A/J mice. More importantly, human lung cancer tissues appear to have elevated LKB1 phosphorylation. Our results reveal, for the first time, that NNAL may promote lung cancer progression through LKB1 deactivation in an isomer-dependent manner.