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Attenuation of sepsis-induced organ injury in mice by vitamin C

Journal of Parenteral and Enteral Nutrition, ISSN: 1941-2444, Vol: 38, Issue: 7, Page: 825-839
2014
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Metabolic Resuscitation Using Ascorbic Acid, Thiamine, and Glucocorticoids in Sepsis.; ORANGES

STUDY INFORMATION OFFICIAL TITLE: Outcomes of Metabolic Resuscitation Using Ascorbic Acid, Thiamine, and Glucocorticoids in the Early Treatment of Sepsis. CURRENT STATUS: Recruiting STUDY TYPE:

Article Description

Background: Multiple organ dysfunction syndrome (MODS) is the principal cause of death in patients with sepsis. Recent work supports the notion that parenteral vitamin C (VitC) is protective in sepsis through pleiotropic mechanisms. Whether suboptimal levels of circulating VitC increase susceptibility to sepsis-induced MODS is unknown. Materials and Methods: Unlike mice, humans lack the ability to synthesize VitC because of loss of L-gulono-γ-lactone oxidase (Gulo), the final enzyme in the biosynthesis of VitC. To examine whether physiological levels of VitC are required for defense against a catastrophic infection, we induced sepsis in VitC sufficient and VitC deficient Gulo-/- mice by intraperitoneal infusion of a fecal stem solution (FIP). Some VitC deficient Gulo-/- mice received a parenteral infusion of ascorbic acid (AscA, 200 mg/kg) 30 minutes after induction of FIP. We used molecular, histological, and biochemical analyses to assess for MODS as well as abnormalities in the coagulation system and circulating blood cells. Results: FIP produced injury to lungs, kidneys and liver (MODS) in VitC deficient Gulo-/- mice. MODS was not evident in FIP-exposed VitC sufficient Gulo-/- mice and attenuated in VitC deficient Gulo-/- mice infused with AscA. Septic VitC deficient Gulo-/- mice developed significant abnormalities in the coagulation system and circulating blood cells. These were attenuated by VitC sufficiency/infusion in septic Gulo-/- mice. Conclusions: VitC deficient Gulo-/- mice were more susceptible to sepsis-induced MODS. VitC sufficiency or parenteral infusion of VitC, following induction of sepsis, normalized physiological functions that attenuated the development of MODS in sepsis.

Bibliographic Details

Fisher, Bernard J; Kraskauskas, Donatas; Martin, Erika J; Farkas, Daniela; Puri, Puneet; Massey, H Davis; Idowu, Michael O; Brophy, Donald F; Voelkel, Norbert F; Fowler, Alpha A; Natarajan, Ramesh

Wiley

Medicine; Nursing

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