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Inflammatory response in microvascular endothelium in sepsis: role of oxidants.

Cepinskas G, Wilson JX - J Clin Biochem Nutr (2008)

Bottom Line: It is characterized by the excessive production of reactive oxygen species (ROS) both in the circulation and in the affected organs.The excessive generation of ROS inevitably leads to oxidative stress in the microvasculature and has been implicated as a causative event in a number of pathologies including sepsis.Changes in microvascular endothelial cells, the cell type that occurs in all organs, are discussed.

View Article: PubMed Central - PubMed

Affiliation: Centre for Critical Illness Research, Lawson Health Research Institute, 800 Commissioners Rd. E., London, Ontario, N6A 4G4, Canada.

ABSTRACT
Sepsis, as a severe systemic inflammatory response to bacterial infection, represents a major clinical problem. It is characterized by the excessive production of reactive oxygen species (ROS) both in the circulation and in the affected organs. The excessive generation of ROS inevitably leads to oxidative stress in the microvasculature and has been implicated as a causative event in a number of pathologies including sepsis. In this review, we focus on the role of oxidative and nitrosative stress during the early onset of sepsis. Changes in microvascular endothelial cells, the cell type that occurs in all organs, are discussed. The mechanisms underlying septic induction of oxidative and nitrosative stresses, the functional consequences of these stresses, and potential adjunct therapies for microvascular dysfunction in sepsis are identified.

No MeSH data available.


Related in: MedlinePlus

Proposed mechanisms by which ascorbate and DHAA may prevent microvascular dysfunction and death in sepsis. The dotted lines represent inhibition by ascorbate of NADPH oxidase (Nox) activity and HIF-1.
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Figure 4: Proposed mechanisms by which ascorbate and DHAA may prevent microvascular dysfunction and death in sepsis. The dotted lines represent inhibition by ascorbate of NADPH oxidase (Nox) activity and HIF-1.

Mentions: As depicted in Fig. 4, ascorbate is transported into microvascular endothelial cells by the specific transporter SVCT2, while DHAA is taken up through facilitative glucose transporters (GLUT) and then reduced to ascorbate [79, 91–93]. The intracellular concentrations of ascorbate thus achieved are 4–16 mM [37, 94]. This intracellular ascorbate may protect microvascular function in two phases of action: initially by inhibiting NADPH oxidase activation and increasing eNOS activity, and subsequently by suppressing expression of NADPH oxidase, iNOS and tissue factor (Fig. 4).


Inflammatory response in microvascular endothelium in sepsis: role of oxidants.

Cepinskas G, Wilson JX - J Clin Biochem Nutr (2008)

Proposed mechanisms by which ascorbate and DHAA may prevent microvascular dysfunction and death in sepsis. The dotted lines represent inhibition by ascorbate of NADPH oxidase (Nox) activity and HIF-1.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2386519&req=5

Figure 4: Proposed mechanisms by which ascorbate and DHAA may prevent microvascular dysfunction and death in sepsis. The dotted lines represent inhibition by ascorbate of NADPH oxidase (Nox) activity and HIF-1.
Mentions: As depicted in Fig. 4, ascorbate is transported into microvascular endothelial cells by the specific transporter SVCT2, while DHAA is taken up through facilitative glucose transporters (GLUT) and then reduced to ascorbate [79, 91–93]. The intracellular concentrations of ascorbate thus achieved are 4–16 mM [37, 94]. This intracellular ascorbate may protect microvascular function in two phases of action: initially by inhibiting NADPH oxidase activation and increasing eNOS activity, and subsequently by suppressing expression of NADPH oxidase, iNOS and tissue factor (Fig. 4).

Bottom Line: It is characterized by the excessive production of reactive oxygen species (ROS) both in the circulation and in the affected organs.The excessive generation of ROS inevitably leads to oxidative stress in the microvasculature and has been implicated as a causative event in a number of pathologies including sepsis.Changes in microvascular endothelial cells, the cell type that occurs in all organs, are discussed.

View Article: PubMed Central - PubMed

Affiliation: Centre for Critical Illness Research, Lawson Health Research Institute, 800 Commissioners Rd. E., London, Ontario, N6A 4G4, Canada.

ABSTRACT
Sepsis, as a severe systemic inflammatory response to bacterial infection, represents a major clinical problem. It is characterized by the excessive production of reactive oxygen species (ROS) both in the circulation and in the affected organs. The excessive generation of ROS inevitably leads to oxidative stress in the microvasculature and has been implicated as a causative event in a number of pathologies including sepsis. In this review, we focus on the role of oxidative and nitrosative stress during the early onset of sepsis. Changes in microvascular endothelial cells, the cell type that occurs in all organs, are discussed. The mechanisms underlying septic induction of oxidative and nitrosative stresses, the functional consequences of these stresses, and potential adjunct therapies for microvascular dysfunction in sepsis are identified.

No MeSH data available.


Related in: MedlinePlus