Oxidative stress after moderate to extensive burning in humans

Citation
Am. Pintaudi et al., Oxidative stress after moderate to extensive burning in humans, FREE RAD RE, 33(2), 2000, pp. 139-146
Citations number
41
Categorie Soggetti
Biochemistry & Biophysics
Journal title
FREE RADICAL RESEARCH
ISSN journal
10715762 → ACNP
Volume
33
Issue
2
Year of publication
2000
Pages
139 - 146
Database
ISI
SICI code
1071-5762(2000)33:2<139:OSAMTE>2.0.ZU;2-I
Abstract
Lipid peroxidation products, lipid antioxidants, and hematologic and blood chemistry changes were evaluated in plasma of patients after acute burning injury involving 10% (n = 8), 20% (n = 8), and 40% (n = 5) of total body su rface area (TBSA), 25 h after burning (baseline) up to 30 days after. Marke dly increased plasma levels of malondialdehyde (MDA) were observed at basel ine in all patients, according to the extent of the injury, then the values declined progressively However, levels of MDA remained above normal up to 30 days ea en in less injured patients. On the other hand, the plasma level of conjugated diene lipid hydroperoxides was only slightly higher than con trol at the baseline, then dropped under the control value in all patients. Cholesterol showed a marked fall at baseline, followed by a rapidly progre ssive decrease, indicating a massive loss of circulating lipids by the acut e thermal injury. Because of such an extensive and rapidly spreading oxidat ive degradation of lipids, decomposition of conjugated diene hydroperoxides , produced in early stages of the peroxidation process, occurs, so these co mpounds cannot be a suitable index to value lipid oxidation in burned patie nts. Aldehydic products of lipid peroxidation act as endotoxins, causing damage to various tissues and organs. Damage to liver and decrease of erythrocyte survival were assessed by increased plasma levels of asparate and alanine t ransaminases, within 7-15 days after injury, and by a decreased number of r ed blood cells, which remained under the normal value at 30 days. A marked decrease of lipid antioxidants, beta-carotene, vitamin A and vitam in E was observed at baseline. The level of beta-carotene remained low in a ll patients at the end of the 30-day observation. A complete recovery of vi tamin A did not occur at 30 days post-burn, even in the patients with 10% o f burned TBSA. Plasma levels of vitamin E decreased significantly in 1-7 da ys after burn in all patients, but these levels increased thereafter, with almost total recovery at 30 days. These data show evidence of a marked, long-lasting oxidant/antioxidant imba lance in burned patients, in accordance with the severity of the injury, wh ich is also reflected as systemic oxidant stress.