The relationship between obesity and oxidant stress parameters has been extensively studied in healthy adults. However, it is unknown whether this relationship exists from early age and if it has the same trends during childhood. The response to oxidant damage caused by ROS production differs from age to age: The maturation of antioxidant enzymes is, in fact, related to ageing. In this study, we examined the variations of antioxidant enzyme activities – considered biomarkers of oxidant stress – in a population of healthy obese children. Cases of endogenic obesity were not considered to exclude other factors influencing the antioxidant enzyme activity [16
]. A control group composed of healthy normal-weight children was established with comparable age and gender-related distributions. Obesity indicators, such as BMI, waist and hip circumferences, were shown to significantly increase in diagnosed obese children. There was also no gender disparity in BMI, waist or hip circumference, in line with previous studies [16
Obesity can be defined as an excess of body fat. There are several methods of measuring the percentage of body fat. In the clinical environment, techniques based on BMI, waist or hip circumference, and skin fold thickness have been extensively used and suggested to be satisfactory in identifying risk [19
]. Some authors [20
] have suggested using waist circumference since it seems to be more accurate for children: it targets central obesity, which is a risk factor for type II diabetes and coronary heart disease.
This study showed that the antioxidant enzyme activity of SOD was markedly higher in the obese children compared to the normal-weight ones, taking into account the gender and the age-related variations. No significant difference was obtained in the second step enzymes (GPx and CAT) activities. These results confirm the fact that obesity is associated with the oxidant stress increase, even in early age. Possible mechanisms contributing to the obesity-associated oxidant stress include increased oxygen consumption and subsequent radical production via mitochondrial respiration, increased fat deposition and cell injury causing increased rates of radical formation [21
]. The cell adaptation to the increase of radical production, as a consequence of obesity, consists then in the increase of SOD activity. In pediatric obesity, only the first-step enzyme (SOD) activity seems to be affected by the increase of body fat. A previous investigation performed on healthy children had also shown that the SOD activity was enhanced in association to obesity [16
]. Other studies on animal and human adults showed controversial results. Koboyasi et al. [22
] demonstrated that the production of superoxide anion and the Cu/ZnSOD activity increased in obese mice. Nakao et al. [23
] also reported significant increased SOD levels in the liver, kidney, muscles, plasma, and white and brown adipose tissues of obese mice. Vincent et al. [21
] found that the Cu/ZnSOD activity in the left ventricles of rats was greater in the obese animals compared to lean controls. Other studies have identified no significant or opposite difference in individual antioxidant enzyme concentrations in obesity. Brown et al. [6
] found no significant difference in total antioxidant status, SOD and reduced glutathione among normal-weight, overweight, and obese adults. On the contrary, Olusi [24
] found that erythrocyte Cu/ZnSOD activity was significantly lower in obese subjects compared to results from control subjects. Similarly, Ozata et al. [25
] reported 42% lower SOD activity in obese vs. non-obese men. These discrepancies could be linked to the duration of obesity. For example, in the development stages of obesity, antioxidant enzymes may be stimulated whereas in chronic and long-term obesity, the sources of antioxidant enzymes become depleted, leading to a low level activity [6
]. An example of antioxidant stimulation during the development stages of obesity has been shown in the study of Dobrian et al. [26
] who reported increases in the activity of SOD after 10 weeks of diet-induced obesity in rats. The effects of chronic obesity has not been scientifically studied but could be achieved by studying obese individuals of similar weight and body composition and varying degrees of length of obesity time.
The anti-oxidant enzyme activity is subject to various stress-related factors, including physical activity and hypercholesterolemia. Woo et al. [27
] investigated the effects of detraining on the antioxidant enzyme in Korean overweight children. They showed, in particular, that the protein and expression of GPx was increased following a 12-week as compared with prior to training. The protein and expression of SOD showed no significant changes. On the other hand, it had been shown that hypercholesterolaemic non-obese children had lower red cell antioxidant enzymes [28
]. As a consequence, they could be more susceptible to the adverse effects of reactive oxygen species. In the present study, these factors have not been considered to investigate separately the effect of obesity on the markers of the antioxidant enzyme activity.
In addition, hyperglycemia, hypertension, and hypercholesterolemia are also possible sources of increased oxidant stress in the obese state [29
]. The present study showed that the antioxidant enzyme defense was enhanced in obese children, which had normal health parameters including blood pressure, glucose, and triglycerides concentrations. Moreover, the associations between the antioxidant enzyme activities and these biochemical data were not significant. This allows rejecting the hypothesis saying that the obesity-associated oxidant stress is only a consequence of obesity-related diseases [30
]. Instead, it can be related to the excess in the adipose tissue accumulation. These findings are also confirmed by Keaney et al. [32
] who found in a community-based cohort, a strong association between markers of oxidant stress and BMI, implicating adiposity as the main factor for increased oxidant stress.
When the plasma levels of total cholesterol of obese and normal-weight children were compared, there was a significant increase in the obese group. Although, both total cholesterol and SOD levels were significantly higher in obese children, no correlation was observed between the two parameters. Free radicals are very potent oxidants and react with lipids to result in lipid peroxidation [33
Although, the general consensus is that obesity (and increased BMI) increases oxidant stress even during childhood, it is difficult to identify a typical-related oxidant stress response because the majority of studies have incorporated different methodology designs including different oxidant stress markers.