Obesity Exacerbates Sepsis-Induced Oxidative Damage in Organs
- PDF / 836,072 Bytes
- 10 Pages / 595.276 x 790.866 pts Page_size
- 51 Downloads / 182 Views
ORIGINAL ARTICLE
Obesity Exacerbates Sepsis-Induced Oxidative Damage in Organs Fabricia Petronilho,1,4 Amanda Della Giustina,1 Diego Zapelini Nascimento,1 Graciela Freitas Zarbato,1 Andriele Aparecida Vieira,1 Drielly Florentino,1 Lucinéia Gainski Danielski,1 Mariana Pereira Goldim,1 Gislaine Tezza Rezin,1 and Tatiana Barichello2,3
Abstract—Sepsis progression is linked to the imbalance between reactive oxygen species and antioxidant enzymes. Sepsis affects multiple organs, but when associated with a chronic inflammatory disease, such as obesity, it may be exacerbated. We hypothesized that obesity could aggravate the oxidative damage to peripheral organs of rats submitted to an animal model of sepsis. Male Wistar rats aged 8 weeks received hypercaloric nutrition for 2 months to induce obesity. Sepsis was induced by cecal ligation and puncture (CLP) procedure, and sham-operated rats were considered as control group. The experimental groups were divided into sham + eutrophic, sham + obese, CLP + eutrophic, and CLP + obese. Twelve and 24 h after surgery, oxidative damage to lipids and proteins and superoxide dismutase (SOD) and catalase (CAT) activities were evaluated in the liver, lung, kidney, and heart. The data indicate that obese rats subjected to sepsis present oxidative stress mainly in the lung and liver. This alteration reflected an oxidative damage to lipids and proteins and an imbalance of SOD and CAT levels, especially 24 h after sepsis. It follows that obesity due to its pro-inflammatory phenotype can aggravate sepsis-induced damage in peripheral organs. KEY WORDS: sepsis; obesity; organs; oxidative stress; inflammation.
INTRODUCTION Sepsis is a major cause of mortality in noncardiac intensive care units and is an important cause of death in both 1
Laboratory of Neurobiology of Inflammatory and Metabolic Processes, Postgraduate Program in Health Sciences, University of South Santa Catarina, Avenida José Acácio Moreira, 787, Tubarao, SC 88704-900, Brazil 2 Center for Experimental Models in Psychiatry, Department of Psychiatry and Behavioral Sciences, The University of Texas Medical School at Houston, Houston, TX, USA 3 Laboratory of Experimental Microbiology, Graduate Program in Health Sciences, Health Sciences Unit, University of Southern Santa Catarina, Criciúma, SC, Brazil 4 To whom correspondence should be addressed at Laboratory of Neurobiology of Inflammatory and Metabolic Processes, Postgraduate Program in Health Sciences, University of South Santa Catarina, Avenida José Acácio Moreira, 787, Tubarao, SC 88704-900, Brazil. E-mail: [email protected]
developed and underdeveloped countries [1–3]. This syndrome is a severe clinical condition as consequence of a systemic inflammatory state with release of endogenous mediators and the triggering of inflammatory cascades due to the occurrence of a suspected or diagnosed infection [4, 5]. Activation of inflammatory cascades through cytokine stimulation of immune and endothelial cells results in increased production of reactive oxygen species
Data Loading...
