a(CHEBI:"carbon monoxide")
Carbon monoxide has vasodilatory, anti-proliferative, anti-inflammatory and antioxidant properties, whereas bilirubin, the product of biliverdin reductase, is an antioxidant (Baranano et al, 2002). PubMed:25307023
Within cells, heme is catabolized by the activity of heme oxygenases (inducible HO-1 and constitutive HO-2) into iron, carbon monoxide, and biliverdin. PubMed:26675351
Pretreating anticoagulated whole blood with tricarbonyldichlororuthenium(II) dimer, a CO donor, significantly reduced collagen exposure (Fig. 5A) and thrombus formation (Fig. 5B) induced by FeCl3. PubMed:19276082
Once inside the cells, heme is catabolized by HO enzymes, generating equimolar amounts of biliverdin, carbon monoxide (CO), and Fe (Tenhunen et al., 1968). PubMed:24904418
The beneficial effects of Hp and Hpx were lost by inhibition of HO with SnPP, but could be restored by CO administration. PubMed:29694434
The beneficial effects of Hp and Hpx were lost by inhibition of HO with SnPP, but could be restored by CO administration. PubMed:29694434
Moreover, mitochondrial translocation of HO-1 can also lead to localized CO production as a result of heme degradation, thus inhibiting electron flow though mitochondrial electron transport chain complex IV (44). PubMed:26974230
SnPP and CO had similar inhibitory effects on NF-kB activation in the liver (data not shown). PubMed:29694434
Figure 5C shows that pretreatment of human RBC stored for 35 days with CO, or CO-added 5 min after H2O2, significantly accelerated Prx-2 reduction from the dimer to monomer (by *35% relative to control at 20 min). PubMed:25264713
CO also inhibited stasis in mice treated with SnPP + Hb without Hp or Hpx. PubMed:29694434
By-products of heme and iron metabolism, such as heme oxygenase-dependent generation of carbon monoxide (CO), have antioxidant and anti-inflammatory protective functions against iron-induced vascular damage (33); therefore we examined the impact of CO donors on collagen exposure and thrombus formation in the ex vivo vascular injury model. PubMed:19276082
Carbon monoxide has vasodilatory, anti-proliferative, anti-inflammatory and antioxidant properties, whereas bilirubin, the product of biliverdin reductase, is an antioxidant (Baranano et al, 2002). PubMed:25307023
Figure 5C shows that pretreatment of human RBC stored for 35 days with CO, or CO-added 5 min after H2O2, significantly accelerated Prx-2 reduction from the dimer to monomer (by *35% relative to control at 20 min). PubMed:25264713
By-products of heme and iron metabolism, such as heme oxygenase-dependent generation of carbon monoxide (CO), have antioxidant and anti-inflammatory protective functions against iron-induced vascular damage (33); therefore we examined the impact of CO donors on collagen exposure and thrombus formation in the ex vivo vascular injury model. PubMed:19276082
Pretreating anticoagulated whole blood with tricarbonyldichlororuthenium(II) dimer, a CO donor, significantly reduced collagen exposure (Fig. 5A) and thrombus formation (Fig. 5B) induced by FeCl3. PubMed:19276082
Differently from biliverdin and CO, which have anti-inflammatory effects (Otterbein et al., 2000; Baranano et al., 2002), free Fe is highly oxidative and can promote free radicals generation through the Fenton reaction, which catalyzes hydroxyl radicals from the reaction of Fe with H2O2 (Fenton, 1894). PubMed:24904418
CO inhibits Hb oxidation and subsequently heme release, thus blocking heme accumulation in serum and preventing heme from exerting its inflammatory effects in the course of malaria disease (Ferreira et al., 2011). PubMed:24904418
Within cells, heme is catabolized by the activity of heme oxygenases (inducible HO-1 and constitutive HO-2) into iron, carbon monoxide, and biliverdin. PubMed:26675351
Presaturation of RBC with CO affected neither initial H2O2- dependent Prx-2 oxidation nor Prx-2 reduction in either RBC, although a trend toward decreased Prx-2 oxidation over 5 min was noted in CO-treated cells ( p = 0.08 between with and without CO groups for b93Cys RBC). PubMed:25264713
This could be explained by the finding that CO induces vasodilation by binding to the heme-protein guanylyl cyclase [67]. PubMed:26368565
Carbon monoxide has vasodilatory, anti-proliferative, anti-inflammatory and antioxidant properties, whereas bilirubin, the product of biliverdin reductase, is an antioxidant (Baranano et al, 2002). PubMed:25307023
Carbon monoxide has vasodilatory, anti-proliferative, anti-inflammatory and antioxidant properties, whereas bilirubin, the product of biliverdin reductase, is an antioxidant (Baranano et al, 2002). PubMed:25307023
Carbon monoxide has vasodilatory, anti-proliferative, anti-inflammatory and antioxidant properties, whereas bilirubin, the product of biliverdin reductase, is an antioxidant (Baranano et al, 2002). PubMed:25307023
Moreover, mitochondrial translocation of HO-1 can also lead to localized CO production as a result of heme degradation, thus inhibiting electron flow though mitochondrial electron transport chain complex IV (44). PubMed:26974230
CO also inhibited stasis in mice treated with SnPP + Hb without Hp or Hpx. PubMed:29694434
SnPP and CO had similar inhibitory effects on NF-kB activation in the liver (data not shown). PubMed:29694434
The beneficial effects of Hp and Hpx were lost by inhibition of HO with SnPP, but could be restored by CO administration. PubMed:29694434
The beneficial effects of Hp and Hpx were lost by inhibition of HO with SnPP, but could be restored by CO administration. PubMed:29694434
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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.