Carotenoids and Antioxidant Nutrients following Burn Injurya

Rock, Cheryl L.; Rodriguez, Jorge Luis; Khilnani, Rubina; Lown, Deborah

doi:10.1111/j.1749-6632.1993.tb26193.x

Cited by 7 publications

(3 citation statements)

References 6 publications

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“…Plasma levels of c~-tocopherol were inversely correlated with the level of the proinflammatory interleukin-8 in burned patients. [13] In addition, vitamin A and vitamin E may affect production of collagen fibers, [4°'411 which could control formation of hypertrophic scars. Maintenance of adequate levels of both vitamins may be advised.…”

Section: Discussionmentioning

confidence: 99%

Oxidative stress after moderate to extensive burning in humans

Pintaudi

Tesoriere

D’Arpa

et al. 2000

Free Radical Research

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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.

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Section: Discussionmentioning

confidence: 99%

Oxidative stress after moderate to extensive burning in humans

Pintaudi

Tesoriere

D’Arpa

et al. 2000

Free Radical Research

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“…[67][68][69] The nonenzymatic antioxidants include mainly ascorbic acid, glutathione, albumin, alpha-tocopherol, uric acid, and β-carotene. [70][71][72] In addition to the increased ROS/RNS (Reactive nitrogen species), asthmatic lungs have lower enzymatic antioxidants such as SODs, catalase, and glutathione peroxidases as well as heme oxygenase-1, thioredoxins, peroxiredoxins, and glutaredoxins. 73 Asthma is characterized by decreased activities of antioxidants.…”

Section: E Viden Ce For the Pre S En Ce Of Oxidative S Tre Ss In A mentioning

confidence: 99%

“…An imbalance of the airway reducing state is a determinant of asthma initiation and severity (Figure ) . The nonenzymatic antioxidants include mainly ascorbic acid, glutathione, albumin, alpha‐tocopherol, uric acid, and β‐carotene . In addition to the increased ROS/RNS (Reactive nitrogen species), asthmatic lungs have lower enzymatic antioxidants such as SODs, catalase, and glutathione peroxidases as well as heme oxygenase‐1, thioredoxins, peroxiredoxins, and glutaredoxins .…”

Section: Evidence For the Presence Of Oxidative Stress In Asthmamentioning

confidence: 99%

Oxidative stress in asthma: Part of the puzzle

Şahiner

Birben

Erzurum

et al. 2018

Pediatric Allergy Immunology

108

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An imbalance between the production of reactive oxygen species and the capacity of antioxidant defense mechanisms favoring oxidants is called oxidative stress and is implicated in asthmatic inflammation and severity. Major reactive oxygen species that are formed endogenously include hydrogen peroxide, superoxide anion, hydroxyl radical, and hypohalite radical; and the major antioxidants that fight against the endogenous and environmental oxidants are superoxide dismutase, catalase, and glutathione. Despite the well-known presence of oxidative stress in asthma, studies that target oxidative burden using a variety of nutritional, pharmacological, and environmental approaches have generally been disappointing. In this review, we summarize the current knowledge on oxidative stress and antioxidant imbalance in asthma. In addition, we focus on possible biomarkers of oxidative stress in asthma and on current and future treatment strategies using the modulation of oxidative stress to treat asthma patients.

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Recombinant human deoxyribonuclease attenuates oxidative stress in a model of eosinophilic pulmonary response in mice

et al. 2016

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The inflammatory cells infiltrating the airways produce several mediators, such as reactive oxygen species (ROS). ROS and the oxidant-antioxidant imbalance might play an important role in the modulation of airways inflammation. In order to avoid the undesirable effects of ROS, various endogenous antioxidant strategies have evolved, incorporating both enzymatic and non-enzymatic mechanisms. Recombinant human deoxyribonuclease (rhDNase) in clinical studies demonstrated a reduction in sputum viscosity, cleaving extracellular DNA in the airways, and facilitating mucus clearance, but an antioxidant effect was not studied so far. Therefore, we evaluated whether the administration of rhDNase improves oxidative stress in a murine model of asthma. Mice were sensitized by two subcutaneous injections of ovalbumin (OVA), on days 0 and 7, followed by three lung challenges with OVA on days 14, 15, and 16. On days 15 and 16, after 2 h of the challenge with OVA, mice received 1 mg/mL of rhDNase in the lungs. Bronchoalveolar lavage fluid and lung tissue were obtained on day 17, for inflammatory and oxidative stress analysis. We showed that rhDNase did not alter the population of inflammatory cells, such as eosinophil cells, in OVA-treated rhDNase group but significantly improved oxidative stress in lung tissue, by decreasing oxygen reactive species and increasing superoxide dismutase/catalase ratio, glutathione peroxidase activity, and thiol content. Our data provide the first evidence that rhDNase decreases some measures of oxidative stress and antioxidant status in a murine model of asthma, with a potential antioxidant effect to be further studied in human asthma.

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Carotenoids and Antioxidant Nutrients following Burn Injurya

Abstract: Carotenoids are among the circulating antioxidant micronutrients, and plasma levels of these compounds generally reflect dietary intake, when possible confounding factors such as body mass are considered. '-* Patients who have suffered

Cited by 7 publications

References 6 publications

Oxidative stress after moderate to extensive burning in humans

Oxidative stress after moderate to extensive burning in humans

Oxidative stress in asthma: Part of the puzzle

Recombinant human deoxyribonuclease attenuates oxidative stress in a model of eosinophilic pulmonary response in mice

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