Synthetic cannabinoids were originally developed by academic and pharmaceutical laboratories with the hope of providing therapeutic relief from the pain of inflammatory and degenerative diseases. However, recreational drug enthusiasts have flushed the market with new strains of these potent drugs that evade detection yet endanger public health and safety. Although many of these drug derivatives were published in the medical literature, others were merely patented without further characterization. AB‐FUBINACA is an example of one of the new indazole‐carboxamide synthetic cannabinoids introduced in the past year. Even though AB‐FUBINACA has become increasingly prominent in forensic drug and toxicology specimens analyses, little is known about the pharmacology of this substance. To study its metabolic fate, we utilized Wistar rats to study the oxidative products of AB‐FUBINACA in urine and its effect on gene expressions in liver and heart. Rats were injected with 5 mg/kg of AB‐FUBINACA each day for 5 days. Urine samples were collected every day at the same time. On day 5 after treatment, we collected the organs such as liver and heart. The urine samples were analyzed by mass spectrometry, which revealed several putative metabolites and positioning of the hydroxyl addition on the molecule. We used quantitative PCR gene expression array to analyze the hepatotoxicity and cardiotoxicity on these rats and confirmed by real‐time quantitative RT‐PCR. We identified three genes significantly associated with dysfunction of oxidation and inflammation. Our study reports in vivo metabolites of AB‐FUBINACA in urine and its effect on the gene expressions in liver and heart. J. Cell. Biochem. 117: 1033–1043, 2016. © 2015 The Authors. Journal of Cellular Biochemistry Published by Wiley Periodicals. Inc.

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The aim of the study is to evaluate the contribution of ethanol metabolite detection in postmortem cases by showing the connection between the presence of ethanol metabolites, which are indicators of alcohol consumption, and the detection of potential postmortem ethanol formation in decomposed and diabetic cases. Determination of ethanol consumption before death is often one of the most important questions in death investigations. Postmortem ethanol formation or degradation products in the blood make it difficult to distinguish antemortem consumption or postmortem formation of ethanol and eventually may lead to misinterpretation. Decomposed bodies and diabetic cases are vulnerable to postmortem ethanol formation due to putrefaction, fermentation or other degradations. Ethyl glucuronide (EtG) and ethyl sulphate (EtS) are two metabolites of ethanol produced only in the antemortem time interval. In this study, EtG and EtS levels in urine and vitreous humor samples of 27 postmortem cases, including diabetic and degraded bodies were compared to ethanol results of their blood, urine, and vitreous humor samples. EtG and EtS in urine and vitreous humor were analyzed by liquid chromatography–tandem mass spectrometry (LC–MS-MS) and ethanol was assayed by routine headspace gas chromatography–flame ionization detector (GC–FID). These cases were devoid of other influences from forensically relevant drugs, so ethanol and/or glucose were among the only positive findings in these cases. The results of this pilot study indicate the postmortem ethanol concentrations do not correlate with the measured EtG and EtS values but are beneficial in rulings of accidental or natural deaths. This preliminary study gives additional data to help distinguish between antemortem ethanol intake and postmortem formation. EtG and EtS were well correlated positively with antemortem ethanol use instead of forming spontaneously in samples from decedents who are decomposing or have a history of diabetic hyperglycemia.

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