Levels of malondialdehyde ( MDA ) and total glutathione to were used to assess oxidative stress.
7. Ling, P. R.; Mueller, C.; Smith, R. J.; Bistrian, B. R.
JOURNAL NAME- Metabolism VOL. 52 2003 Jul PP. 868-74 DOCUMENT TYPE- Journal Article ISSN- 0026-0495 CORPORATE
AUTHOR- Nutrition/Infection Laboratory, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston,
MA 02215, USA. PUBLICATION COUNTRY- United States LANGUAGE- English The purpose of this study was to determine
the effects of acute hyperglycemia induced by glucose infusion on oxidative stress, systemic inflammation, and
several key signal intermediates in liver for the systemic inflammatory response in nonstressed rats. Rats
received saline or glucose infusion (hyperglycemic clamp) for 3 hours. Rats without catheter insertion were
included as an additional control for observing the effects of surgical stress. Levels of malondialdehyde (
MDA ) and total glutathione to assess oxidative stress were determined in liver and muscle. Proinflammatory
cytokines including tumor necrosis factor (TNF), interleukin (IL)-1 and IL-6, and alpha 1 acid glycoprotein
(alpha1-AG) were determined in serum. The protein content and phosphorylation of extracellular
signal-regulated kinase (ERK)1/2, p38 stress-activated protein kinase (p38), and signal transducer and
activator of transcription-3 (STAT-3) were examined in the liver tissue with or without IL-6 stimulation. The
results showed that acute hyperglycemia significantly increased MDA release and depleted total glutathione in
liver but not in muscle. Hyperglycemia also significantly elevated the production of TNF, IL-1, and alpha1-AG,
but not IL-6 in serum. However, hyperglycemia for 3 hours in vivo did not activate ERK1/2, p38 and STAT3 in
liver, and also did not alter the response of these signal proteins to IL-6 stimulation. These data suggest
that acute (3 hours) hyperglycemia causes hepatic oxidative stress and activates a low-grade systemic
inflammation but does not affect key components of the IL-6 signaling pathway in liver.
Return from Free Radical Reference 7 Malondialdehyde
to Free Radical Laboratory Validation 1.