Topic
Hemin
About: Hemin is a research topic. Over the lifetime, 2919 publications have been published within this topic receiving 90653 citations.
Papers published on a yearly basis
1 / 2
Papers
TL;DR: In vitro and in vivo results provide genetic evidence that up-regulation of Hmox1 serves as an adaptive mechanism to protect cells from oxidative damage during stress.
Abstract: Stressed mammalian cells up-regulate heme oxygenase 1 (Hmox1; EC 1.14.99.3), which catabolizes heme to biliverdin, carbon monoxide, and free iron. To assess the potential role of Hmox1 in cellular antioxidant defense, we analyzed the responses of cells from mice lacking functional Hmox1 to oxidative challenges. Cultured Hmox1−/− embryonic fibroblasts demonstrated high oxygen free radical production when exposed to hemin, hydrogen peroxide, paraquat, or cadmium chloride, and they were hypersensitive to cytotoxicity caused by hemin and hydrogen peroxide. Furthermore, young adult Hmox1−/− mice were vulnerable to mortality and hepatic necrosis when challenged with endotoxin. Our in vitro and in vivo results provide genetic evidence that up-regulation of Hmox1 serves as an adaptive mechanism to protect cells from oxidative damage during stress.
1,350 citations
TL;DR: The aptamer-hemin complexes described are novel DNA enzymes and their study will help elucidate the structural and functional requirements of peroxidase enzymes in general and the ways that a nucleic acid 'apoenzyme' might work to enhance the intrinsicPeroxidatic ability of hemin.
947 citations
TL;DR: This perspective reviews the principal mechanisms of Hb and hemin toxicity in different disease states, updates how the natural scavengers efficiently control these toxic moieties, and explores critical issues in the development of human plasma-derived Hp and hemopexin as therapeutics for patients with excessive intravascular hemolysis.
702 citations
TL;DR: This paper demonstrated for the first time a simple wet-chemical strategy for synthesizing hemin-graphene hybrid nanosheets (H-GNs) through the π-π interactions and developed a label-free colorimetric detection system for single-nucleotide polymorphisms (SNPs) in disease-associated DNA.
Abstract: This paper demonstrated for the first time a simple wet-chemical strategy for synthesizing hemin−graphene hybrid nanosheets (H-GNs) through the π−π interactions. Significantly, this new material possesses the advantages of both hemin and graphene and exhibits three interesting properties. First, H-GNs have intrinsic peroxidase-like activity, which can catalyze the reaction of peroxidase substrate, due to the existence of hemin on the graphene surface. Second, their dispersion follow the 2D Schulze−Hardy rule, that is to say, the coagulation of H-GNs in electrolyte solution results from the interplay between van der Waals attraction and electric double-layer repulsion. Third, H-GNs exhibit the ability to differentiate ss- and ds-DNA in optimum electrolyte concentration, owing to the different affinities of ss- and ds-DNA to the H-GNs. On the basis of these unique properties of the as-prepared H-GNs, we have developed a label-free colorimetric detection system for single-nucleotide polymorphisms (SNPs) in d...
596 citations
TL;DR: Hemin and CO-releasing molecules (CORM) promote Erastin-induced ferroptotic cell death, not by biliverdin and bilirubin, but by hemin and CORM accelerate the HO-1 expression in the presence of Erastsin and increase membranous lipid peroxidation.
Abstract: The oncogenic RAS-selective lethal small molecule Erastin triggers a unique iron-dependent form of nonapoptotic cell death termed ferroptosis. Ferroptosis is dependent upon the production of intracellular iron-dependent reactive oxygen species (ROS), but not other metals. However, key regulators remain unknown. The heme oxygenase (HO) is a major intracellular source of iron. In this study, the role of heme oxygenase in Erastin-triggered ferroptotic cancer cell death has been investigated. Zinc protoporphyrin IX (ZnPP), a HO-1 inhibitor, prevented Erastin-triggered ferroptotic cancer cell death. Furthermore, Erastin induced the protein and mRNA levels of HO-1 in HT-1080 fibrosarcoma cells. HO-1+/+ and HO-1-/- fibroblast, HO-1 overexpression, and chycloheximide-treated experiments revealed that the expression of HO-1 has a decisive effects in Erastin-triggered cell death. Hemin and CO-releasing molecules (CORM) promote Erastin-induced ferroptotic cell death, not by biliverdin and bilirubin. In addition, hemin and CORM accelerate the HO-1 expression in the presence of Erastin and increase membranous lipid peroxidation. Thus, HO-1 is an essential enzyme for iron-dependent lipid peroxidation during ferroptotic cell death.
547 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 2026 | 2 |
| 2025 | 51 |
| 2024 | 120 |
| 2023 | 163 |
| 2022 | 239 |
| 2021 | 93 |