J Korean Soc Emerg Med.  1999 Dec;10(4):522-530.

Effects of Vitamin-C on Sepsis Rat Model Induced by Endotoxin

Abstract

BACKGROUND: Multi-organ failure from sepsis is very lethal disease entity, which is suspected to be caused by activated inflammatory cells. Inflammatory cells activated by endotoxins generate oxidants and cytokines such as TNF-alpha and IL-6, which in turn stimulate macrophages and neutrophils. Augmented inflammation makes an organ-injury deteriorate into an organ-failure, which may progress to multi-organ failure. This study is designed to evaluate the therapeutic effects of vitamin-C, a scavenger of oxidants, in sepsis.
METHODS
Male Sprague-Dawley rats were divided into 3 groups : a control group, a group injected intrapetoneally with LPS(lipopolysaccharide), and a group injected intraperitoneally with LPS and vitamin-C. Each eight rats were sacrified 24 hours and 48 hours after injection, and samples of the blood, the liver and the lung were obtained. Biochemical assays of TNF-alpha level in the blood and malondialdehyde(MDA) level, catalase activity and nitric oxide synthase(NOS) activity in the liver and the lung tissues were performed.
RESULTS
Serum TNF-alpha level, tissue lipid peroxidation and tissue i-NOS activity were dramatically increased, and tissue catalase activity was exhausted rapidly in sepsis. High dose vitamin-C administration decreased serum TNF-alpha level, tissue lipid peroxidation and tissue i-NOS induction, and protected against catalase exhaustion.
CONCLUSION
high dose vitamin-C therapy was proved to have definite antioxidant effect in septic condition.


MeSH Terms

Animals
Antioxidants
Catalase
Cytokines
Endotoxins
Humans
Inflammation
Interleukin-6
Lipid Peroxidation
Liver
Lung
Macrophages
Male
Models, Animal*
Neutrophils
Nitric Oxide
Oxidants
Rats*
Rats, Sprague-Dawley
Sepsis*
Tumor Necrosis Factor-alpha
Antioxidants
Catalase
Cytokines
Endotoxins
Interleukin-6
Nitric Oxide
Oxidants
Tumor Necrosis Factor-alpha
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