PMID- 24433072
OWN - NLM
STAT- MEDLINE
DCOM- 20141215
LR  - 20220317
IS  - 1557-7600 (Electronic)
IS  - 1096-620X (Print)
IS  - 1096-620X (Linking)
VI  - 17
IP  - 5
DP  - 2014 May
TI  - Citric acid effects on brain and liver oxidative stress in 
      lipopolysaccharide-treated mice.
PG  - 588-98
LID - 10.1089/jmf.2013.0065 [doi]
AB  - 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 mug/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-alpha) 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-alpha, 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.
FAU - Abdel-Salam, Omar M E
AU  - Abdel-Salam OM
AD  - 1 Department of Toxicology and Narcotics, National Research Center , Cairo, 
      Egypt.
FAU - Youness, Eman R
AU  - Youness ER
FAU - Mohammed, Nadia A
AU  - Mohammed NA
FAU - Morsy, Safaa M Youssef
AU  - Morsy SM
FAU - Omara, Enayat A
AU  - Omara EA
FAU - Sleem, Amany A
AU  - Sleem AA
LA  - eng
PT  - Journal Article
DEP - 20140116
PL  - United States
TA  - J Med Food
JT  - Journal of medicinal food
JID - 9812512
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antioxidants)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Nitrites)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 2968PHW8QP (Citric Acid)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 3.1.8.1 (Aryldialkylphosphatase)
RN  - EC 3.4.22.- (Caspase 3)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents
MH  - Antioxidants
MH  - Aryldialkylphosphatase/analysis
MH  - Brain/drug effects/metabolism
MH  - Brain Chemistry/drug effects
MH  - Caspase 3/analysis
MH  - Citric Acid/*therapeutic use
MH  - DNA Fragmentation/drug effects
MH  - Glutathione Peroxidase/analysis
MH  - Inflammation/chemically induced/*drug therapy/metabolism
MH  - Lipid Peroxidation
MH  - Lipopolysaccharides/*administration & dosage
MH  - Liver/chemistry/drug effects/*metabolism
MH  - Liver Diseases/prevention & control
MH  - Male
MH  - Mice
MH  - Nitric Oxide Synthase Type II/analysis
MH  - Nitrites/analysis
MH  - Oxidative Stress/*drug effects
MH  - Peritoneum/drug effects
MH  - Tumor Necrosis Factor-alpha/analysis
PMC - PMC4026104
OTO - NOTNLM
OT  - antioxidant activity
OT  - citric acid
OT  - cytokines
OT  - dietary supplementation
OT  - peripheral infection
OT  - systemic inflammation
EDAT- 2014/01/18 06:00
MHDA- 2014/12/17 06:00
PMCR- 2015/05/01
CRDT- 2014/01/18 06:00
PHST- 2014/01/18 06:00 [entrez]
PHST- 2014/01/18 06:00 [pubmed]
PHST- 2014/12/17 06:00 [medline]
PHST- 2015/05/01 00:00 [pmc-release]
AID - 10.1089/jmf.2013.0065 [pii]
AID - 10.1089/jmf.2013.0065 [doi]
PST - ppublish
SO  - J Med Food. 2014 May;17(5):588-98. doi: 10.1089/jmf.2013.0065. Epub 2014 Jan 16.