Lipid peroxidation and antioxidant enzyme status in various tissues of mice with gold-thioglucose-induced obesity.

Abstract

SummaryTo determine whether an oxidant-antioxidant imbalance exists in the non-genetic obese model, we induced obesity in 3-week-old female ICR mice by gold-thioglucose administration, and the lipid peroxide level and activities of antioxidant enzymes were measured in the plasma, liver, heart, and skeletal muscle. Two types of superoxide dismutase were assayed by radioimmunoassays. Lipid peroxide was estimated from fluorimetric measurement of thiobarbituric acid-reactive substances (TBARS). The plasma levels of both cholesterol (Chol) and triacylglycerol (TG) and liver TG content were increased in the obese mice. The superoxide dismutases were unaltered, while the activities of both glutathione peroxidase and catalase in the obese liver and heart were decreased. Lipid peroxide levels were unaltered in the obese liver and heart, decreased in the skeletal muscle, and increased in the plasma. The body weight correlated positively with the liver weight, heart weight, liver TG, liver Chol, plasma TG, plasma Chol, and plasma TBARS, and inversely with the tissue levels of some of the antioxidant enzymes and TBARS. The tissue levels of the antioxidant enzymes and TBARS had a general tendency to decrease in the obese animals. These results suggest that oxidative stress is enhanced only in the plasma of the obese mice and not in any of the tissues studied here. lism produces an accumulative deleterious change in mitochondrial function at a rate related to the rate of oxygen consumption, leading to the aging of the cells [1]. According to this hypothesis, food restriction decreases oxygen consumption, and, in turn, free radical production, resulting in a decreased rate of progression of degenerative disorders including lipid peroxidation [2]. We previously demonstrated that prolonged fasting suppressed mitochondrial oxidative metabolism and lipid peroxidation in certain rat tissues [3]. Conversely, increased food consumption accompanying obesity can enhance oxidative stress, thereby accelerating the degeneration process. Obesity is known to be an independent risk factor of atherosclerosis [4], and the latter process is postulated to be accelerated by an increase in the level of circulating lipid peroxides [5]. Thus, study of the oxidant-antioxidant balance in obesity is of clinical importance. However, little is known about the oxidantantioxidant status in obesity, and data are limited to the genetically obese ob/ob mouse [6][7][8][9]. Abnormal metabolism of trace metals, which is not directly linked to excessive weight gain, is reported to exist in the ob/ob mouse [10]. Such deviation in trace metal status per se may modify tissue levels of antioxidant enzymes, which contain trace metals in their active centers, independently of energy metabolism.To determine whether an oxidant-antioxidant imbalance exists in the nongenetic model of obesity, the obese condition was induced by gold-thioglucose administration to mice, and the lipid peroxide level and activities of antioxidant enzymes were measured in various tissues. MATERI...