Carbon monoxide: Impact on remethylation/transsulfuration metabolism and its pathophysiologic implications
Takako Hishiki, Takehiro Yamamoto, Takayuki Morikawa, Akiko Kubo, Mayumi Kajimura, Makoto Suematsu
Clinical and Translational Research Center
Abstract Carbon monoxide (CO) is a gaseous product generated by heme oxygenase (HO), which oxidatively degrades heme. While the stress-inducible HO-1 has well been recognized as an anti-oxidative defense mechanism under stress conditions, recent studies suggest that cancer cells utilize the reaction for their survival. HO-2, the constitutive isozyme, also plays protective roles as a tonic regulator for neurovascular function. Although protective roles of the enzyme reaction and CO have extensively been studied, little information is available on the molecular mechanisms by which the gas exerts its biological actions. Recent studies using metabolomics revealed that CO inhibits cystathionine β-synthase (CBS), which generates H2S, another gaseous mediator. The CO-dependent CBS inhibition may impact on the remethylation cycle and related metabolic pathways including the methionine salvage pathway and polyamine synthesis. This review focuses on the gas-responsive regulation of metabolic systems, particularly the remethylation and transsulfuration pathways, and their putative implications for cancer and ischemic diseases.
Published - 2012 Mar
Cystathionine
Heme Oxygenase (Decyclizing)
Heme Oxygenase-1
Metabolic Networks and Pathways
Isoenzymes
Cystathionine β-synthase
Gas biology
Metabolic systems
Methionine salvage pathway
Hishiki, T., Yamamoto, T., Morikawa, T., Kubo, A., Kajimura, M., & Suematsu, M. (2012). Carbon monoxide: Impact on remethylation/transsulfuration metabolism and its pathophysiologic implications. Journal of Molecular Medicine, 90(3), 245-254. https://doi.org/10.1007/s00109-012-0875-2
Carbon monoxide : Impact on remethylation/transsulfuration metabolism and its pathophysiologic implications. / Hishiki, Takako; Yamamoto, Takehiro; Morikawa, Takayuki; Kubo, Akiko; Kajimura, Mayumi; Suematsu, Makoto.
In: Journal of Molecular Medicine, Vol. 90, No. 3, 03.2012, p. 245-254.
Hishiki, T, Yamamoto, T, Morikawa, T, Kubo, A, Kajimura, M & Suematsu, M 2012, 'Carbon monoxide: Impact on remethylation/transsulfuration metabolism and its pathophysiologic implications', Journal of Molecular Medicine, vol. 90, no. 3, pp. 245-254. https://doi.org/10.1007/s00109-012-0875-2
Hishiki T, Yamamoto T, Morikawa T, Kubo A, Kajimura M, Suematsu M. Carbon monoxide: Impact on remethylation/transsulfuration metabolism and its pathophysiologic implications. Journal of Molecular Medicine. 2012 Mar;90(3):245-254. https://doi.org/10.1007/s00109-012-0875-2
Hishiki, Takako ; Yamamoto, Takehiro ; Morikawa, Takayuki ; Kubo, Akiko ; Kajimura, Mayumi ; Suematsu, Makoto. / Carbon monoxide : Impact on remethylation/transsulfuration metabolism and its pathophysiologic implications. In: Journal of Molecular Medicine. 2012 ; Vol. 90, No. 3. pp. 245-254.
@article{162edbfb10124f23acfdbc2c78a6ad29,
title = "Carbon monoxide: Impact on remethylation/transsulfuration metabolism and its pathophysiologic implications",
abstract = "Abstract Carbon monoxide (CO) is a gaseous product generated by heme oxygenase (HO), which oxidatively degrades heme. While the stress-inducible HO-1 has well been recognized as an anti-oxidative defense mechanism under stress conditions, recent studies suggest that cancer cells utilize the reaction for their survival. HO-2, the constitutive isozyme, also plays protective roles as a tonic regulator for neurovascular function. Although protective roles of the enzyme reaction and CO have extensively been studied, little information is available on the molecular mechanisms by which the gas exerts its biological actions. Recent studies using metabolomics revealed that CO inhibits cystathionine β-synthase (CBS), which generates H2S, another gaseous mediator. The CO-dependent CBS inhibition may impact on the remethylation cycle and related metabolic pathways including the methionine salvage pathway and polyamine synthesis. This review focuses on the gas-responsive regulation of metabolic systems, particularly the remethylation and transsulfuration pathways, and their putative implications for cancer and ischemic diseases.",
keywords = "Cancer, Cystathionine β-synthase, Epigenetics, Gas biology, Glutathione, Heme oxygenase, Hydrogen sulfide, Metabolic systems, Methionine salvage pathway, Methylation",
author = "Takako Hishiki and Takehiro Yamamoto and Takayuki Morikawa and Akiko Kubo and Mayumi Kajimura and Makoto Suematsu",
journal = "Journal of Molecular Medicine",
T1 - Carbon monoxide
T2 - Impact on remethylation/transsulfuration metabolism and its pathophysiologic implications
AU - Hishiki, Takako
AU - Yamamoto, Takehiro
AU - Morikawa, Takayuki
AU - Kubo, Akiko
AU - Kajimura, Mayumi
AU - Suematsu, Makoto
N2 - Abstract Carbon monoxide (CO) is a gaseous product generated by heme oxygenase (HO), which oxidatively degrades heme. While the stress-inducible HO-1 has well been recognized as an anti-oxidative defense mechanism under stress conditions, recent studies suggest that cancer cells utilize the reaction for their survival. HO-2, the constitutive isozyme, also plays protective roles as a tonic regulator for neurovascular function. Although protective roles of the enzyme reaction and CO have extensively been studied, little information is available on the molecular mechanisms by which the gas exerts its biological actions. Recent studies using metabolomics revealed that CO inhibits cystathionine β-synthase (CBS), which generates H2S, another gaseous mediator. The CO-dependent CBS inhibition may impact on the remethylation cycle and related metabolic pathways including the methionine salvage pathway and polyamine synthesis. This review focuses on the gas-responsive regulation of metabolic systems, particularly the remethylation and transsulfuration pathways, and their putative implications for cancer and ischemic diseases.
AB - Abstract Carbon monoxide (CO) is a gaseous product generated by heme oxygenase (HO), which oxidatively degrades heme. While the stress-inducible HO-1 has well been recognized as an anti-oxidative defense mechanism under stress conditions, recent studies suggest that cancer cells utilize the reaction for their survival. HO-2, the constitutive isozyme, also plays protective roles as a tonic regulator for neurovascular function. Although protective roles of the enzyme reaction and CO have extensively been studied, little information is available on the molecular mechanisms by which the gas exerts its biological actions. Recent studies using metabolomics revealed that CO inhibits cystathionine β-synthase (CBS), which generates H2S, another gaseous mediator. The CO-dependent CBS inhibition may impact on the remethylation cycle and related metabolic pathways including the methionine salvage pathway and polyamine synthesis. This review focuses on the gas-responsive regulation of metabolic systems, particularly the remethylation and transsulfuration pathways, and their putative implications for cancer and ischemic diseases.
KW - Cancer
KW - Cystathionine β-synthase
KW - Epigenetics
KW - Gas biology
KW - Glutathione
KW - Heme oxygenase
KW - Hydrogen sulfide
KW - Metabolic systems
KW - Methionine salvage pathway
KW - Methylation
JO - Journal of Molecular Medicine
JF - Journal of Molecular Medicine