4.3 Article

Dehydroascorbic acid as pre-conditioner: Protection from lipopolysaccharide induced mitochondrial damage

Journal

FREE RADICAL RESEARCH
Volume 44, Issue 3, Pages 283-292

Publisher

TAYLOR & FRANCIS LTD
DOI: 10.3109/10715760903468766

Keywords

Vitamin C; reactive oxygen species; monocyte; endotoxin; mitochondria; pre-conditioning

Funding

  1. MRC [G0800149] Funding Source: UKRI
  2. Medical Research Council [G0800149] Funding Source: Medline
  3. Medical Research Council [G0800149] Funding Source: researchfish

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Oxidative stress-induced mitochondrial dysfunction is a common consequence of severe sepsis. However, oxidative stress also activates signalling cascades which enable protection of cells against subsequent oxidative damage. This study hypothesized that cellular uptake of vitamin C as dehydroascorbic acid rather than ascorbic acid would up-regulate antioxidant enzyme systems and impart a protective effect to mitochondria in cells subsequently exposed to lipopolysaccharide (LPS) in an iron free environment. Treatment of monocytes with dehydroascorbic acid, but not ascorbic acid, caused oxidative stress (p < 0.001). Dehydroascorbic acid exposure also resulted in increased manganese superoxide dismutase (p= 0.018) and catalase (p= 0.003) expression. Pre-treatment of monocytes with dehydroascorbic acid followed by LPS resulted in higher mitochondrial membrane potentials than cells without pre-treatment (p < 0.0001). Lower cytochrome c in cytosol (p < 0.05) and higher mitochondrial expression of the anti-apoptotic Bcl-2 protein (p= 0.029) was also found in monocytes pre-treated before subsequent LPS exposure, compared to cells without pre-treatment. In conclusion, acute exposure of monocytes to dehydroascorbic acid in an iron free environment induces cytoprotective antioxidant enzymes and protected mitochondria from the harmful effects of oxidative stress prior to a septic insult, which was abrogated when cells were pre-incubated with the DHA uptake inhibitor cytocholasin B.

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