Decreased membrane fluidity and altered susceptibility to peroxidation and lipid composition in overweight and obese female erythrocytes

• Published in: Journal of lipid research Vol. 45; no. 10; pp. 1846 - 1851
• Main Authors: Cazzola, Roberta, Rondanelli, Mariangela, Russo-Volpe, Samantha, Ferrari, Ettore, Cestaro, Benvenuto
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.10.2004; Elsevier
• Subjects: Adult; Body Mass Index; Case-Control Studies; erythrocytes; Erythrocytes - chemistry; Erythrocytes - metabolism; essential fatty acids; Female; fluorescence anisotropy; Free Radicals; Glutathione - metabolism; Hemolysis; Humans; Lipid Peroxidation; Lipids - analysis; Lipids - classification; membrane cholesterol; Membrane Fluidity; obesity; Obesity - blood; overweight; Oxidation-Reduction; Oxidative Stress; fluorescence anisotropy; membrane cholesterol; oxidative stress; essential fatty acids
• ISSN: 0022-2275; 1539-7262
• DOI: 10.1194/jlr.M300509-JLR200

The increased generation of reactive oxygen species that occurs in the condition of obesity may be responsible for oxidative injury to erythrocyte membranes, which could lead to a decrease in tissue oxygenation. Therefore, we have looked into the effects of obesity on both indexes of oxidative damage and physical-chemical properties of erythrocyte membranes in 50 overweight or obese [25 < body mass index (BMI) < 33], normotensive, nondiabetic women and 50 age-matched lean healthy women (BMI < 25). In the obese group compared with the lean group, we found that a) the onset of free radical-induced erythrocyte hemolysis and the ratio between reduced and oxidized glutathione were reduced, whereas the rate of free radical-induced damage increased; b) the n-3 fatty acid and the phospholipid contents decreased; c) the ratio between cholesterol and phospholipids increased; and d) the membrane fluidity decreased. These findings suggest an impairment of erythrocyte membrane physical-chemical properties in overweight and obese people as a consequence of oxidative injury that might be part of a pathogenetic mechanism responsible for obesity-related pathologies such as atherosclerosis and hypertension.