Date de publication: 2013Télécharger
Obesity has become a major health problem in both developed and under-developed countries. It is a complex disease that involves the interactions between environmental  and genetic factors . The prevalence of obesity has increased at an alarming rate during the last three decades, and has been particularly problematic in children. The main direct adverse effects of childhood obesity include orthopedic complications, sleep apnea, and psychological disorders . Approximately 70% of obese adolescents grow up to become obese adults . Defining the basic physiopathology of childhood obesity should be the first step in preventing the associated consequences that may develop lifelong. In particular, the cellular defense mechanisms and their influence against many diseases were thought to be related to obesity and its complications as seen in adults . Cells have developed an enzymatic antioxidant pathway against reactive oxygen species (ROS) that are generated during oxidative metabolism: first, the dismutation of superoxide anion (O2 - ) to hydrogen peroxide (H2O2) catalyzed by superoxide dismutase (SOD); and then, the conversion of H2O2 to H2O by glutathione peroxidase (GPx) or catalase (CAT). The activity of first- and second-step antioxidant enzymes must be balanced to prevent oxidative damage in cells, which may contribute to various pathological processes . Compared to adult studies, the knowledge about the response to oxidant stress damage caused by obesity during childhood is limited. The present work aimed at investigating the effect of the childhood obesity on the antioxidant enzyme activities (SOD, GPx and CAT).