Arakawa, Koichi published the artcileFunctional modulation of liver mitochondria in lipopolysaccharide/drug co-treated rat liver injury model, Computed Properties of 97-67-6, the main research area is liver mitochondria lipopolysaccharide injury rat; Diclofenac; Drug-induced liver injury; Lipopolysaccharide; Mitochondria; Mitochondrial permeability transition.
Drug-induced liver injury is not readily detectable using conventional animal studies during pre-clin. drug development. To address this problem, other researchers have proposed the use of co-administration of lipopolysaccharide (LPS), an endotoxin produced by gram-neg. bacteria, and a drug. Using this approach, liver injury that is otherwise not detected following drug administration alone can be successfully identified. Previous studies have demonstrated that such injury is suppressed by heparin; therefore, the mechanism may involve coagulation-dependent ischemia. However, it has not been established how LPS-induced ischemia might sensitize hepatocytes to a potentially hepatotoxic drug. In the present study, we aimed to determine the effect of LPS-induced ischemia on liver mitochondrial function and downstream toxicol. responses. Consistent with previous findings, plasma alanine transaminase (ALT) activity was higher in rats co-administered with LPS (1 mg/kg) and diclofenac (100 mg/kg), but reduced by heparin. Liver mRNA expression of Hmox1 encoding heme oxygenase-1, an oxidative stress indicator, was three times higher at 2 h after LPS administration. Furthermore, respiratory activity via mitochondrial complex II, lipid peroxidation in mitochondria, and the susceptibility to mitochondrial permeability transition pore opening in response to diclofenac administration were significantly increased by LPS administration. The increase in plasma ALT activity and the sensitization to mitochondrial permeability transition pore opening were reduced by the co-administration of heparin. In conclusion, LPS-induced transient ischemia disrupts respiratory chain complex activities, enhances reactive oxygen species production, especially in mitochondria, and sensitizes mitochondria to permeability transition pore opening when testing a potentially hepatotoxic drug in vivo.
Journal of Toxicological Sciences published new progress about Animal gene, CXCL10 Role: BSU (Biological Study, Unclassified), BIOL (Biological Study). 97-67-6 belongs to class alcohols-buliding-blocks, name is (S)-2-hydroxysuccinic acid, and the molecular formula is C4H6O5, Computed Properties of 97-67-6.
Referemce:
Alcohol – Wikipedia,
Alcohols – Chemistry LibreTexts