Effect of ammonium fluoride as a mobile phase additive on quantitativity of fatty acids in electrospray ionization-liquid chromatography-tandem mass spectrometry.

Fatty acids (FAs) are essential molecules in biological systems and have crucial roles for fundamental components of cellular membranes, energy stores and mediators for cellular functions. The growing importance of FAs has also paid attention to analytical methods for the determination of FA contents in various samples accurately. Liquid chromatography tandem mass spectrometry (LC-MS/MS) analysis is a powerful tool due to less time for sample preparation and analysis.

Inhibitory Effects of Lysophospholipids on Survival and Interleukin-8 Secretion of HT-29, a Human Colon Cancer-Derived Epithelial Cell.

Lysophpsphospholipids (LPLs) are lipid mediators involved in various physiological functions. In daily diets, people consume large amounts of various lipids, including LPLs. Exogenous dietary LPLs initially affect epithelial cells and, finally, the entire colon and may be linked to the onset and prevention of colonic diseases, including inflammatory bowel disease.

Enhanced expression of Cyp17a1 and production of DHEA-S in the liver of late-pregnant rats.

Cytochrome P450 17A1 (CYP17A1) catalyzes two enzymatic reactions in the biosynthesis of dehydroepiandrosterone (DHEA) from pregnenolone. In pregnant humans, the adrenal gland is responsible for DHEA biosynthesis, which is then sulfated by SULT2A1 and released into the bloodstream. This sulfated DHEA is subsequently taken up by the placenta and deconjugated to serve as a precursor for estrogen biosynthesis.

DNA methylation of Ad4BP/SF-1 suppresses Cyp11a1 and StAR transcripts in C2C12 myoblasts.

Steroidogenesis occurs locally in peripheral tissues and via adrenal and gonadal glands' biosynthesis. The C2C12 mouse myoblast cell line and rat skeletal muscles harbor a local steroidogenesis pathway for glucocorticoids, and corticosterone is biosynthesized from skeletal muscle cells. However, Cyp11a1 and StAR protein expressions are not observed in C2C12 cells or rat muscular tissues.

Establishment of hyperoxic cell culture system for predicting drug-induced liver injury: reducing accumulated lipids in hepatocytes derived from chimeric mice with humanized liver.

Drug-induced liver injury (DILI) is a major adverse reaction. Species-specific differences between humans and laboratory animals make it difficult to establish evaluation models that can accurately predict DILI in the preclinical phase. Chimeric mice with humanized liver are potential predictive models for understanding DILI.

Inhibition of cytochrome P450 3A protein degradation and subsequent increase in enzymatic activity through p38 MAPK activation by acetaminophen and salicylate derivatives.

Cytochrome P450 (CYP) 3A4 plays an important role in drug metabolism. Although transcriptional regulation of CYP3A expression by chemicals has been comprehensively studied, its post-translational regulation is not fully understood. We previously reported that acetaminophen (APAP) caused accumulation of functional CYP3A protein via inhibition of CYP3A protein degradation through reduction of glycoprotein 78 (gp78), an E3 ligase of the ubiquitin proteasome system.

Acetaminophen analog N-acetyl-m-aminophenol, but not its reactive metabolite, N-acetyl-p-benzoquinone imine induces CYP3A activity via inhibition of protein degradation.

Cytochrome P450 (CYP) 3A subfamily members are known to metabolize various types of drugs, highlighting the importance of understanding drug-drug interactions (DDI) depending on CYP3A induction or inhibition. While transcriptional regulation of CYP3A members is widely understood, post-translational regulation needs to be elucidated. We previously reported that acetaminophen (APAP) induces CYP3A activity via inhibition of protein degradation and proposed a novel DDI concept.