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KMID : 1161420140170050588
Journal of Medicinal Food
2014 Volume.17 No. 5 p.588 ~ p.598
Citric Acid Effects on Brain and Liver Oxidative Stress in Lipopolysaccharide-Treated Mice
Abdel-Salam Omar M. E.

Youness Eman R.
Mohammed Nadia A.
Morsy Safaa M. Youssef
Omara Enayat A.
Sleem Amany A.
Abstract
Citric acid is a weak organic acid found in the greatest amounts in citrus fruits. This study examined the effect of citric acid on endotoxin-induced oxidative stress of the brain and liver. Mice were challenged with a single intraperitoneal dose of lipopolysaccharide (LPS; 200 ¥ìg/kg). Citric acid was given orally at 1, 2, or 4?g/kg at time of endotoxin injection and mice were euthanized 4?h later. LPS induced oxidative stress in the brain and liver tissue, resulting in marked increase in lipid peroxidation (malondialdehyde [MDA]) and nitrite, while significantly decreasing reduced glutathione, glutathione peroxidase (GPx), and paraoxonase 1 (PON1) activity. Tumor necrosis factor-alpha (TNF-¥á) showed a pronounced increase in brain tissue after endotoxin injection. The administration of citric acid (1?2?g/kg) attenuated LPS-induced elevations in brain MDA, nitrite, TNF-¥á, GPx, and PON1 activity. In the liver, nitrite was decreased by 1?g/kg citric acid. GPx activity was increased, while PON1 activity was decreased by citric acid. The LPS-induced liver injury, DNA fragmentation, serum transaminase elevations, caspase-3, and inducible nitric oxide synthase expression were attenuated by 1?2?g/kg citric acid. DNA fragmentation, however, increased after 4?g/kg citric acid. Thus in this model of systemic inflammation, citric acid (1?2?g/kg) decreased brain lipid peroxidation and inflammation, liver damage, and DNA fragmentation.
KEYWORD
antioxidant activity, citric acid, cytokines, dietary supplementation, peripheral infection, systemic inflammation
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