Catalysts are substances that increase the reaction rate of a chemical reaction without being consumed in the process. 123-08-0, Name is 4-Hydroxybenzaldehyde, SMILES is O=CC1=CC=C(O)C=C1, belongs to indole-building-block compound. In a document, author is Schuran, Fenja A., introduce the new discover, HPLC of Formula: https://www.ambeed.com/products/123-08-0.html.
BACKGROUND & AIMS: Acetaminophen (APAP)-induced liver injury is one of the most common causes of acute liver failure, however, a dear definition of sensitizing risk factors is lacking. Here, we investigated the role of the ligand-activated transcription factor aryl hydrocarbon receptor (Ahr) in APAP-induced liver injury. We hypothesized that Ahr, which integrates environmental, dietary, microbial and metabolic signals into complex cellular transcriptional programs, might act as a rheostat for APAP-toxicity. METHODS: Wildtype or conditional Ahr knockout mice lacking Ahr in hepatocytes (Alb(Delta/Delta Ahr)) or myeloid cells (LysM(Delta/Delta Ahr)) were treated with the specific Ahr ligand 2-(1’H-indole-3′-carbonyl)-thiazole-4-carboxylic acid methyl ester (ITE) together with APAP. RESULTS: Ahr activation by ITE, which by itself was non-toxic, exacerbated APAP-induced hepatotoxicity compared to vehicle-treated controls, causing 80% vs. 0% mortality after administration of a normally sublethal APAP overdose. Of note, Ahr activation induced hepatocyte death even at APAP doses within the therapeutic range. Aggravated liver injury was associated with significant neutrophil infiltration; however, lack of Ahr in myeloid cells did not protect LysM(Delta/Delta Ahr) mice from exacerbated APAP hepatotoxicity. In contrast, Alb(Delta/Delta Ahr) mice were largely protected from ITE-induced aggravated liver damage, indicating that Ahr activation in hepatocytes, but not in myeloid cells, was instrumental for disease exacerbation. Mechanistically, Ahr activation fueled hepatic accumulation of toxic APAP metabolites by up-regulating expression of the APAP-metabolizing enzyme Cyp1a2, a direct Ahr downstream target. CONCLUSIONS: Ahr activation in hepatocytes potentiates APAP-induced hepatotoxicity. Thus, individual exposition to environmental Ahr ligands might explain individual sensitivity to hyperacute liver failure.
The proportionality constant is the rate constant for the particular unimolecular reaction. the reaction rate is directly proportional to the concentration of the reactant. I hope my blog about 123-08-0 is helpful to your research. HPLC of Formula: https://www.ambeed.com/products/123-08-0.html.
Reference:
Indole alkaloid derivatives as building blocks of natural products from Bacillus thuringiensis and Bacillus velezensis and their antibacterial and antifungal activity study,
,Preparation of Indole Containing Building Blocks for the Regiospecific Construction of Indole Appended Pyrazoles and Pyrroles