Ask about this productRelated genes to: CYP1A2 antibody
- Gene:
- CYP1A2 NIH gene
- Name:
- cytochrome P450 family 1 subfamily A member 2
- Previous symbol:
- -
- Synonyms:
- P3-450, CP12
- Chromosome:
- 15q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-04-25
- Date modifiied:
- 2019-04-23
Related products to: CYP1A2 antibody
Related articles to: CYP1A2 antibody
- Kashin-Beck disease (KBD) is a multifactorial endemic osteoarthropathy that has been associated with nutritional and environmental factors, including selenium deficiency and T-2 toxin exposure. However, whether combined selenium deficiency and T-2 toxin exposure affects hepatic xenobiotic metabolism has not been systematically investigated. Male C57BL/6 mice were fed a selenium-adequate or selenium-deficient diet for 4 weeks, followed by another 4 weeks with or without daily oral T-2 toxin (0.2 mg/kg). Plasma selenium and glutathione peroxidase (GPx) activity were measured. Hepatic histology, activities of major mouse cytochrome P450 (Cyp450) isoforms, and corresponding mRNA and protein expression were assessed. RNA sequencing was performed using liver samples from four biological replicates per group to identify differentially expressed genes (DEGs) and enriched pathways. Selenium deficiency was confirmed by significantly reduced plasma selenium levels and GPx activity. Histological examination revealed marked hepatic steatosis. Transmission electron microscopy further showed prominent ultrastructural alterations including endoplasmic reticulum dilation. The activities of five hepatic Cyp450 isoforms, Cyp1a2, Cyp2b10, Cyp2c29, Cyp2c50, and Cyp3a11, were significantly increased to 1.64-2.51 times the control levels, consistent with increased mRNA and protein expression. Combined selenium deficiency and T-2 toxin exposure was associated with increased hepatic Cyp450 enzyme activity and expression, identifying the liver as a responsive target of KBD-related exposures. These findings suggest the need to further evaluate hepatic xenobiotic metabolism in populations from KBD-endemic areas. - Source: PubMed
Publication date: 2026/09/04
Zhao TongZhao YichenMao TingtingDa WeixuanQin LinaLiu LiLiu HuanCheng BolunWen YanZhang FengJia Yumeng - The aryl hydrocarbon receptor (AHR) is a central mediator of cellular responses to environmental exposures, including cigarette smoke. Appropriate selection of in vitro hepatic models is critical for investigating AHR-dependent induction of xenobiotic-metabolizing enzymes. Therefore, The aim of this study was to compare AHR-mediated induction of CYP1A1 and CYP1A2 across five human hepatic in vitro models to identify the most suitable model. Primary human hepatocytes (PHH), HepaRG, HepG2, HuH-7, and upcyte® hepatocytes were exposed to cigarette smoke extract and prototypical CYP inducers, responses were assessed at mRNA and enzyme activity levels. PHH confirmed their role as gold standard model, while HepaRG cells emerged as practical and ethical alternative for mechanistic studies. HepG2 and HuH-7 showed limited responsiveness. Upcyte® hepatocytes displayed strongly elevated fold changes, compared to other models. Overall, pronounced model-specific differences in AHR responsiveness emphasize the importance of informed in vitro model selection for exposure-relevant studies. By directly contrasting transcript and functional activity endpoints across five models, this work clarifies strengths and limitations that are often not apparent in single-model studies. Therefore, this work provides practical guidance for informed model selection in studies of the AHR signaling pathway. - Source: PubMed
Publication date: 2026/09/04
Lenich Ann-KathrinReindl Lisa-MarieRuez Stephanie - 2,2',4,4'-Tetrabromodiphenyl ether (BDE-47) is a persistent food-chain pollutant targeting the liver, whose genotoxic potential remains poorly understood. Here we investigated BDE-47-triggered DNA damage using HepG2 cells and C3H/He mice. BDE-47 exposure markedly elevated DNA damage-related γ-H2AX foci in mouse liver. Cellular tests further validated BDE-47-induced DNA damage, manifested as elevated γ-H2AX foci, a higher comet tail DNA percentage, and a longer tail length. Mechanistically, BDE-47 activated the aryl hydrocarbon receptor (AHR) and raised hepatic reactive oxygen species (ROS) and malondialdehyde levels. In cellular assays, antioxidants alleviated DNA damage, whereas AHR inhibitors suppressed ROS overproduction. BDE-47 also upregulated hepatic CYP1A1/2, whose expression positively correlated with the severity of hepatic DNA injury in mice. In conclusion, BDE-47 exposure induces hepatocellular DNA damage, and its mechanism of action is closely associated with AHR-mediated oxidative stress and CYP1A1/2 upregulation, which offers new experimental evidence to clarify the hepatotoxic and genotoxic mechanisms of BDE-47. - Source: PubMed
Zhong HuajunYang LiuYang JieqiuHuang SuliBian DongyuanYu YangyangHuang ShijianDeng WeiSu YumengChen ChulinLin Guimiao - Harmane (HAR) is a beta-carboline alkaloid found in plants, heat-processed foods, and tobacco. It is an active component of widely used antidepressant and anxiolytic herbs. In this study, we investigate the effects of HAR on rat CYP enzymes both and and examine the interactions between HAR and human CYP enzymes through methods. - Source: PubMed
Publication date: 2026/08/17
Klásková EZendulka OPeš OEyrilmez S MBednář DJuřica J - Rivoceranib, a vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor with antitumor activity, is metabolized in the liver mostly by cytochrome P450 (CYP)3A4/5. In vitro studies suggest that rivoceranib at clinically relevant concentrations may inhibit metabolism of various CYP substrates. This study evaluated the effects of rivoceranib 200 mg once daily (QD) on the pharmacokinetics of various CYP substrates using the Cooperstown 5+1 cocktail. The dosing regimen of rivoceranib used in this study is similar to the proposed rivoceranib regimen (250 mg QD) in combination with camrelizumab for the treatment of patients with hepatocellular carcinoma. - Source: PubMed
Publication date: 2026/08/29
Nguyen DavidWei Xiaohui TraceyMeng XianzhangAlexander LauraRyan KristinJang Seong