PMID- 22007252
OWN - NLM
STAT- MEDLINE
DCOM- 20120208
LR  - 20211020
IS  - 1740-2530 (Electronic)
IS  - 1740-2522 (Print)
IS  - 1740-2522 (Linking)
VI  - 2012
DP  - 2012
TI  - Deranged bioenergetics and defective redox capacity in T lymphocytes and 
      neutrophils are related to cellular dysfunction and increased oxidative stress in 
      patients with active systemic lupus erythematosus.
PG  - 548516
LID - 10.1155/2012/548516 [doi]
LID - 548516
AB  - Urinary excretion of N-benzoyl-glycyl-Nepsilon-(hexanonyl)lysine, a biomarker of 
      oxidative stress, was higher in 26 patients with active systemic lupus 
      erythematosus (SLE) than in 11 non-SLE patients with connective tissue diseases 
      and in 14 healthy volunteers. We hypothesized that increased oxidative stress in 
      active SLE might be attributable to deranged bioenergetics, defective 
      reduction-oxidation (redox) capacity, or other factors. We demonstrated that, 
      compared to normal cells, T lymphocytes (T) and polymorphonuclear neutrophils 
      (PMN) of active SLE showed defective expression of facilitative glucose 
      transporters GLUT-3 and GLUT-6, which led to increased intracellular basal 
      lactate and decreased ATP production. In addition, the redox capacity, including 
      intracellular GSH levels and the enzyme activity of glutathione peroxidase 
      (GSH-Px) and gamma-glutamyl-transpeptidase (GGT), was decreased in SLE-T. Compared to 
      normal cells, SLE-PMN showed decreased intracellular GSH levels, and GGT enzyme 
      activity was found in SLE-PMN and enhanced expression of CD53, a coprecipitating 
      molecule for GGT. We conclude that deranged cellular bioenergetics and defective 
      redox capacity in T and PMN are responsible for cellular immune dysfunction and 
      are related to increased oxidative stress in active SLE patients.
FAU - Li, Ko-Jen
AU  - Li KJ
AD  - Department of Internal Medicine, National Taiwan University Hospital and National 
      Taiwan University College of Medicine, 7 Chung-Shan South Road, Taipei 100, 
      Taiwan.
FAU - Wu, Cheng-Han
AU  - Wu CH
FAU - Hsieh, Song-Chou
AU  - Hsieh SC
FAU - Lu, Ming-Chi
AU  - Lu MC
FAU - Tsai, Chang-Youh
AU  - Tsai CY
FAU - Yu, Chia-Li
AU  - Yu CL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20111011
PL  - Egypt
TA  - Clin Dev Immunol
JT  - Clinical & developmental immunology
JID - 101183692
RN  - 0 (Biomarkers)
RN  - 0 (Glucose Transport Proteins, Facilitative)
RN  - 0 (Glucose Transporter Type 3)
RN  - 0 (SLC2A9 protein, human)
RN  - EC 1.11.1.9 (Glutathione Peroxidase)
RN  - EC 2.3.2.2 (gamma-Glutamyltransferase)
RN  - K3Z4F929H6 (Lysine)
SB  - IM
MH  - Adolescent
MH  - Adult
MH  - Biomarkers/urine
MH  - Energy Metabolism
MH  - Female
MH  - Gene Expression Regulation, Enzymologic
MH  - Glucose Transport Proteins, Facilitative/genetics
MH  - Glucose Transporter Type 3/genetics/metabolism
MH  - Glutathione Peroxidase/genetics/metabolism
MH  - Humans
MH  - Lupus Vasculitis, Central Nervous 
      System/diagnosis/*immunology/pathology/physiopathology
MH  - Lysine/analogs & derivatives/urine
MH  - Male
MH  - Neutrophils/immunology/*metabolism/pathology
MH  - *Oxidation-Reduction
MH  - *Oxidative Stress
MH  - T-Lymphocytes/immunology/*metabolism/pathology
MH  - gamma-Glutamyltransferase/genetics/metabolism
PMC - PMC3191817
EDAT- 2011/10/19 06:00
MHDA- 2012/02/09 06:00
PMCR- 2011/10/11
CRDT- 2011/10/19 06:00
PHST- 2011/04/30 00:00 [received]
PHST- 2011/06/23 00:00 [revised]
PHST- 2011/07/12 00:00 [accepted]
PHST- 2011/10/19 06:00 [entrez]
PHST- 2011/10/19 06:00 [pubmed]
PHST- 2012/02/09 06:00 [medline]
PHST- 2011/10/11 00:00 [pmc-release]
AID - 10.1155/2012/548516 [doi]
PST - ppublish
SO  - Clin Dev Immunol. 2012;2012:548516. doi: 10.1155/2012/548516. Epub 2011 Oct 11.