Related Products of 120-78-5, The transformation of simple hydrocarbons into more complex and valuable products via catalytic C¨CH bond functionalisation has revolutionised modern synthetic chemistry. 120-78-5, Name is 2,2-Dithiobis(benzothiazole), SMILES is C1(SSC2=NC3=CC=CC=C3S2)=NC4=CC=CC=C4S1, belongs to thiazoles compound. In a article, author is Schuran, Fenja A., introduce new discover of the category.
Aryl Hydrocarbon Receptor Activity in Hepatocytes Sensitizes to Hyperacute Acetaminophen-Induced Hepatotoxicity in Mice
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.
Related Products of 120-78-5, Each elementary reaction can be described in terms of its molecularity, the number of molecules that collide in that step. The slowest step in a reaction mechanism is the rate-determining step.you can also check out more blogs about 120-78-5.
Reference:
Thiazole | C3H3NS – PubChem,
,Thiazole | chemical compound | Britannica