https://scholars.lib.ntu.edu.tw/handle/123456789/540833
標題: | 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 | 作者: | KO-JEN LI CHENG-HAN WU SONG-CHOU HSIEH Lu, Ming-Chi Tsai, Chang-Youh CHIA-LI YU |
公開日期: | 2012 | 卷: | 2012 | 來源出版物: | Clinical and Developmental Immunology | 摘要: | Urinary excretion of N-benzoyl-glycyl-N-(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 -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. Copyright ? 2012 Ko-Jen Li et al. |
URI: | https://www.scopus.com/inward/record.uri?eid=2-s2.0-84855181178&doi=10.1155%2f2012%2f548516&partnerID=40&md5=a5890e950645c201233f6f2685088410 https://scholars.lib.ntu.edu.tw/handle/123456789/540833 |
ISSN: | 1740-2522 | DOI: | 10.1155/2012/548516 | SDG/關鍵字: | 8 hydroxydeoxyguanosine; adenosine triphosphate; amino acid derivative; azathioprine; CD53 antigen; creatinine; gamma glutamyltransferase; glucose transporter; glucose transporter 3; glucose transporter 6; glutathione; glutathione peroxidase; hydroxychloroquine; lactic acid; n benzoylglycyl n epsilon(hexanoyl)lysine; prednisolone; unclassified drug; biological marker; drug derivative; gamma glutamyltransferase; glucose transporter; glucose transporter 3; glutathione peroxidase; lysine; SLC2A9 protein, human; adult; article; bioenergy; controlled study; disease activity; disease duration; enzyme activity; fatty acid oxidation; female; glucose transport; human; human cell; major clinical study; male; neutrophil; oxidation reduction state; oxidative stress; priority journal; protein expression; systemic lupus erythematosus; T lymphocyte; urinary excretion; adolescent; brain vasculitis; energy metabolism; gene expression regulation; genetics; immunology; metabolism; oxidation reduction reaction; oxidative stress; pathology; pathophysiology; urine; Adolescent; Adult; Biological Markers; Energy Metabolism; Female; gamma-Glutamyltransferase; Gene Expression Regulation, Enzymologic; Glucose Transport Proteins, Facilitative; Glucose Transporter Type 3; Glutathione Peroxidase; Humans; Lupus Vasculitis, Central Nervous System; Lysine; Male; Neutrophils; Oxidation-Reduction; Oxidative Stress; T-Lymphocytes |
顯示於: | 醫學系 |
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