One of the major reasons for studying chemical kinetics is to use measurements of the macroscopic properties of a system, Formula: C34H32ClFeN4O4, In homogeneous catalysis, catalysts are in the same phase as the reactants. In a article, mentioned the application of 16009-13-5, Name is Hemin, molecular formula is C34H32ClFeN4O4
Aims: Heme oxygenase-1 (HO-1), an endogenous cytoprotective enzyme, is reported that can be localized in mitochondria under stress, contributing to preserve mitochondrial function. Mitochondrial quality control (QC) is essential to cellular health and recovery linked with redox homeostasis. Recent studies reported that phosphoglycerate mutase family member (PGAM) 5, a mitochondria-resident phosphatase, plays critical role in mitochondrial homeostasis. Therefore, we aim to investigate cytoprotective mechanisms of HO-1 in I/R-induced hepatic injury focusing on mitochondrial QC associated with PGAM5 signaling. Main methods: Mice were subjected to 60 min of hepatic ischemia followed by 6 h reperfusion and were pretreated twice with hemin (HO-1 inducer, 30 mg/kg) or zinc protoporphyrin (ZnPP; HO-1 inhibitor, 10 mg/kg) 16 and 3 h before ischemia. Key findings: I/R increased hepatic and mitochondrial HO activity, which was augmented by hemin. I/R-induced hepatocellular and mitochondrial damages were attenuated by hemin and augmented by ZnPP. Meanwhile, I/R increased mitochondrial biogenesis, as evidenced by increased mitochondrial DNA contents and mitochondrial transcription factor A protein expression. Hemin augmented these results. I/R impaired mitophagy, as indicated by decreases in Parkin protein expression and the number of mitophagic vacuoles. These changes were attenuated by hemin. Hemin attenuated the I/R-induced increase in mitochondrial fission-related protein, dynamin-related protein 1, and the decrease in PGAM5 protein expression. Furthermore, PGAM5 siRNA abolished the effect of HO-1 on mitochondrial QC in HepG2 cells subjected to hypoxia/reoxygenation. Significance: Our findings suggest that HO-1 protects against I/R-induced hepatic injury via regulation of mitochondrial QC by PGAM5 signaling.
The result showed that such a combination of chemo- and biocatalysis improved the catalytic yield more than two times compared with that of sole metal catalysis. We will look forword to the important role of 16009-13-5, and how the biochemistry of the body works.Formula: C34H32ClFeN4O4
Reference：
Iron Catalysis in Organic Synthesis | Chemical Reviews,
Iron Catalysis in Organic Synthesis: A Critical Assessment of What It Takes To Make This Base Metal a Multitasking Champion