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Oxidative stress after moderate to extensive burning in humans.
Free Radic Res 2000; 33(2):139-46FR

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 surface area (TBSA), 24 h after burning (baseline) up to 30 days after. Markedly increased plasma levels of malondialdehyde (MDA) were observed at baseline 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 even in less injured patients. On the other hand, the plasma level of conjugated diene lipid hydroperoxides was only slightly higher than control at the baseline, then dropped under the control value in all patients. Cholesterol showed a marked fall at baseline, followed by a rapidly progressive decrease, indicating a massive loss of circulating lipids by the acute thermal injury. Because of such an extensive and rapidly spreading oxidative degradation of lipids, decomposition of conjugated diene hydroperoxides, produced in early stages of the peroxidation process, occurs, so these compounds cannot be a suitable index to value lipid oxidation in burned patients. 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 transaminases, within 7-15 days after injury, and by a decreased number of red blood cells, which remained under the normal value at 30 days. A marked decrease of lipid antioxidants, beta-carotene, vitamin A and vitamin E was observed at baseline. The level of beta-carotene remained low in all patients at the end of the 30-day observation. A complete recovery of vitamin A did not occur at 30 days post-burn, even in the patients with 10% of burned TBSA. Plasma levels of vitamin E decreased significantly in 1-7 days 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 imbalance in burned patients, in accordance with the severity of the injury, which is also reflected as systemic oxidant stress.

Authors+Show Affiliations

Dipartimento di Farmacochimico Tossicologico e Biologico, Universitá di Palermo, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

10885621

Citation

Pintaudi, A M., et al. "Oxidative Stress After Moderate to Extensive Burning in Humans." Free Radical Research, vol. 33, no. 2, 2000, pp. 139-46.
Pintaudi AM, Tesoriere L, D'Arpa N, et al. Oxidative stress after moderate to extensive burning in humans. Free Radic Res. 2000;33(2):139-46.
Pintaudi, A. M., Tesoriere, L., D'Arpa, N., D'Amelio, L., D'Arpa, D., Bongiorno, A., ... Livrea, M. A. (2000). Oxidative stress after moderate to extensive burning in humans. Free Radical Research, 33(2), pp. 139-46.
Pintaudi AM, et al. Oxidative Stress After Moderate to Extensive Burning in Humans. Free Radic Res. 2000;33(2):139-46. PubMed PMID: 10885621.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Oxidative stress after moderate to extensive burning in humans. AU - Pintaudi,A M, AU - Tesoriere,L, AU - D'Arpa,N, AU - D'Amelio,L, AU - D'Arpa,D, AU - Bongiorno,A, AU - Masellis,M, AU - Livrea,M A, PY - 2000/7/8/pubmed PY - 2001/2/28/medline PY - 2000/7/8/entrez SP - 139 EP - 46 JF - Free radical research JO - Free Radic. Res. VL - 33 IS - 2 N2 - 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 surface area (TBSA), 24 h after burning (baseline) up to 30 days after. Markedly increased plasma levels of malondialdehyde (MDA) were observed at baseline 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 even in less injured patients. On the other hand, the plasma level of conjugated diene lipid hydroperoxides was only slightly higher than control at the baseline, then dropped under the control value in all patients. Cholesterol showed a marked fall at baseline, followed by a rapidly progressive decrease, indicating a massive loss of circulating lipids by the acute thermal injury. Because of such an extensive and rapidly spreading oxidative degradation of lipids, decomposition of conjugated diene hydroperoxides, produced in early stages of the peroxidation process, occurs, so these compounds cannot be a suitable index to value lipid oxidation in burned patients. 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 transaminases, within 7-15 days after injury, and by a decreased number of red blood cells, which remained under the normal value at 30 days. A marked decrease of lipid antioxidants, beta-carotene, vitamin A and vitamin E was observed at baseline. The level of beta-carotene remained low in all patients at the end of the 30-day observation. A complete recovery of vitamin A did not occur at 30 days post-burn, even in the patients with 10% of burned TBSA. Plasma levels of vitamin E decreased significantly in 1-7 days 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 imbalance in burned patients, in accordance with the severity of the injury, which is also reflected as systemic oxidant stress. SN - 1071-5762 UR - https://www.unboundmedicine.com/medline/citation/10885621/full_citation L2 - http://www.tandfonline.com/doi/full/10.1080/10715760000300691 DB - PRIME DP - Unbound Medicine ER -