angielski
https://www.ncbi.nlm.nih.gov/pmc/art...hms-151756.pdf
Mechanism of action of vitamin C in sepsis: Ascorbate modulates
redox signaling in endothelium
John X. Wilson*
Department of Exercise and Nutrition Sciences, University at Buffalo, Buffalo, NY, USA
Abstract
Circulating levels of vitamin C (ascorbate) are low in patients with sepsis. Parenteral administration
of ascorbate raises plasma and tissue concentrations of the vitamin and may decrease morbidity. In
animal models of sepsis, intravenous ascorbate injection increases survival and protects several
microvascular functions, namely, capillary blood flow, microvascular permeability barrier, and
arteriolar responsiveness to vasoconstrictors and vasodilators. The effects of parenteral ascorbate on
microvascular function are both rapid and persistent. Ascorbate quickly accumulates in
microvascular endothelial cells, scavenges reactive oxygen species, and acts through
tetrahydrobiopterin to stimulate nitric oxide production by endothelial nitric oxide synthase. A major
reason for the long duration of the improvement in microvascular function is that cells retain high
levels of ascorbate, which alter redox-sensitive signaling pathways to diminish septic induction of
NADPH oxidase and inducible nitric oxide synthase. These observations are consistent with the
hypothesis that microvascular function in sepsis may be improved by parenteral administration of
ascorbate as an adjuvant therapy