Background: Oxidative stress is an important pathogenetic mechanism in several diseases, and antioxidant supplementation may reduce morbidity and mortality. The aim of this review is to focus on the role of oxidative stress in the pathogenesis and clinical outcome of critical illness, cancer, and neurological disorders and to evaluate the efficacy of antioxidant supplementation on morbidity and mortality in these conditions. Methods: We reviewed the literature on reactive oxygen species and antioxidants in critically ill, neurological, and neoplastic patients. Results and conclusions: Clinical and experimental evidence demonstrates that oxidative stress and/or antioxidant deficiency contribute to morbidity and mortality in critically ill, neurological, and cancer patients. Nutritional and pharmacological approaches to modulate oxidative stress are beneficial in improving clinical outcome in critically ill (especially respiratory distress syndrome) patients. In contrast, antioxidant supplementation does not substantially reduce the risk of cancer in clinical trials and paradoxically beta carotene has been shown to increase cancer risk in heavy smokers. Increased reactive oxygen species production may be exploited to induce apoptosis and to cure selected types of cancer. In dementia, modulation of oxidative stress by vitamin E administration has failed to provide clinical benefits; other oral antioxidants (lipoic acid and n-acetylcysteine) are currently under investigation. (Nutritional Therapy & Metabolism 2009; 27: 62-72). © SINPE-GASAPE.

Reactive oxygen species and antioxidants: Implications for clinical nutrition / M., Zanetti; G., Biolo; R., Biffp; N. E., Deutz; F. W., Guglielmi; A., Palmo; P., Singer; R., Tetamo; Muscaritoli, Maurizio. - In: NUTRITIONAL THERAPY & METABOLISM. - ISSN 1828-6232. - STAMPA. - 27:2(2009), pp. 62-72.

Reactive oxygen species and antioxidants: Implications for clinical nutrition

MUSCARITOLI, Maurizio
2009

Abstract

Background: Oxidative stress is an important pathogenetic mechanism in several diseases, and antioxidant supplementation may reduce morbidity and mortality. The aim of this review is to focus on the role of oxidative stress in the pathogenesis and clinical outcome of critical illness, cancer, and neurological disorders and to evaluate the efficacy of antioxidant supplementation on morbidity and mortality in these conditions. Methods: We reviewed the literature on reactive oxygen species and antioxidants in critically ill, neurological, and neoplastic patients. Results and conclusions: Clinical and experimental evidence demonstrates that oxidative stress and/or antioxidant deficiency contribute to morbidity and mortality in critically ill, neurological, and cancer patients. Nutritional and pharmacological approaches to modulate oxidative stress are beneficial in improving clinical outcome in critically ill (especially respiratory distress syndrome) patients. In contrast, antioxidant supplementation does not substantially reduce the risk of cancer in clinical trials and paradoxically beta carotene has been shown to increase cancer risk in heavy smokers. Increased reactive oxygen species production may be exploited to induce apoptosis and to cure selected types of cancer. In dementia, modulation of oxidative stress by vitamin E administration has failed to provide clinical benefits; other oral antioxidants (lipoic acid and n-acetylcysteine) are currently under investigation. (Nutritional Therapy & Metabolism 2009; 27: 62-72). © SINPE-GASAPE.
2009
antioxidants; artificial nutrition; cancer; critically ill; neurological; oxidative stress
01 Pubblicazione su rivista::01a Articolo in rivista
Reactive oxygen species and antioxidants: Implications for clinical nutrition / M., Zanetti; G., Biolo; R., Biffp; N. E., Deutz; F. W., Guglielmi; A., Palmo; P., Singer; R., Tetamo; Muscaritoli, Maurizio. - In: NUTRITIONAL THERAPY & METABOLISM. - ISSN 1828-6232. - STAMPA. - 27:2(2009), pp. 62-72.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11573/458187
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