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J Surg Res ; 153(2): 224-30, 2009 May 15.
Article in English | MEDLINE | ID: mdl-18952228

ABSTRACT

OBJECTIVE: To investigate the effect of parenteral administration of vitamin C on neutrophil apoptosis by determining Fas receptor expression and caspase-3, poly (ADP-ribose) polymerase (PARP), and Bcl-2 levels in neutrophils from septic abdominal surgery patients. STUDY DESIGN: Twenty septic abdominal surgery patients were studied in a prospective, randomized, double-blinded clinical trial. A group of healthy volunteers (n = 10) constituted a reference group for baseline parameter values. The patients were randomly assigned to a vitamin C-treated (n = 10) or placebo-treated (n = 10) group. For a 6-d period from 12 h post-surgery, the vitamin C group received 450 mg/d of the vitamin in 3 doses and the placebo group an identical administration of 5% dextrose. Early-morning peripheral blood samples were obtained daily from 24 h after vitamin C administration until d 6 post-surgery (T1d-T6d). RESULTS: Vitamin C group showed a nonsignificant reduction in Fas (CD95) expression on CD15-positive peripheral blood neutrophils, significantly decreased caspase-3, and PARP levels (caspase-3: T4d: P < 0.05, T5d: P < 0.05, T6d P < 0.01; and PARP: T3d: P < 0.05, T4d: P < 0.05, T6d: P < 0.05), and significantly increased Bcl-2 levels (T3d: P = 0.001) versus placebo group. CONCLUSIONS: Postoperative vitamin C treatment of septic abdominal surgery patients exerts an antiapoptotic effect on peripheral blood neutrophils, reducing caspase-3 and PARP levels, and increasing Bcl-2 levels. However, these antiapoptotic effects are not maintained at all time points.


Subject(s)
Antioxidants/pharmacology , Apoptosis/drug effects , Ascorbic Acid/pharmacology , Neutrophils/drug effects , Sepsis/surgery , Aged , Caspase 3/metabolism , Digestive System Surgical Procedures , Double-Blind Method , Female , Humans , Male , Middle Aged , Poly(ADP-ribose) Polymerases/metabolism , Postoperative Care , Prospective Studies , Proto-Oncogene Proteins c-bcl-2/metabolism , fas Receptor/metabolism
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