*7.3. CAT*

The peroxisome part of many cells contains the enzyme CAT, which effectively reduces hydrogen peroxide to water. As mentioned earlier, both CAT and GPX are sensitive to H2O2. These two enzymes are exposed to high and low H2O2 concentrations, respectively. For this reason, the concentration of free radicals determines the importance of the two enzymes GPX and CAT [98].

Another way to measure ROS is to observe changes in the antioxidant defense system. Tools such as Total Antioxidant Status (TAS), Trolex Equivalent Antioxidant Capacity (TEAC), Total Radical Trapping Antioxidant Parameter (TRAP), Plasma Iron Reduction Capacity (FRAP), and Radical Oxygen Absorption Capacity (ORAC) can measure antioxidant capacity [41].

#### **8. Obesity, OS, and Antioxidant Supplementation**

Because obesity is more associated with physical inactivity and overeating, genetics play a very limited role in causing the disease. Therefore, for the treatment of obesity, special attention should be paid to the lifestyle because this disease can be prevented and even treated by lifestyle modification [73,99,100]. As mentioned, one of the most important treatment strategies and, of course, prevention of various diseases, especially obesity, is exercise. Multiple studies have shown that AT reserves are reduced by regulating exerciseinduced lipase regulation, which ultimately leads to weight loss and obesity treatment. Another important role of exercise is to create antioxidant profiles, which can be a key solution to further reduce body fat due to OS [61]. The results of various studies show the depletion of both enzymatic and non-enzymatic antioxidant systems. However, the type of tissue and the degree of obesity is among the factors that play an important role in the rate of discharge of these systems [30].

These enzymes protect the body's cells by catalyzing free radicals into water. Various studies have shown that Prxs expression in humans and obese animals is closely related to OS induced by AT. The activity of this enzyme decreases with obesity. On the other hand, PRDXS in adipocytes can increase and decrease lipolytic and lipogenic gene expression, respectively [101]. Scientists have studied the effects of antioxidant supplements on the improvement of obesity caused by OS in various studies. These studies' results are contradictory, and further studies in this field are still required to reach a correct and logical conclusion. For example, vitamin E is one of the supplements for which the usefulness or harmfulness in treating obesity or other metabolic disorders remains unclear [30].

Simán et al. (1996) examined the effect of consuming an antioxidant diet containing butylated hydroxytoluene (BHT 0.5% and 1%) with or without vitamin E acetate (4%) for four weeks in 30 female Sprague Dawley rats. They concluded no change in the alphatocopherol concentration of abdominal AT with BHT supplementation [102]. In another study, Rodrigues et al. (2020) examined the effect of consuming an antioxidant fruit called chestnut at a dose of 1.1% in 18 FVB/Nn male 7-month-old mice. They concluded that this supplement reduced adipose tissue, serum cholesterol, and adipose tissue deposition [103].

Furthermore, Candiracci et al. (2014) investigated the effect of consuming an antioxidant source of rice bran enzymatic extract for 20 weeks in obese and lean Zucker rats. This study's results included the reduction of overproduction of IL-6, TNF-α, IL-1β, and NOS in abdominal and epidermal visceral AT. In addition, reducing the adipocyte size of abdominal and epidural visceral AT was another effect of this supplement on AT [29]. In a study, Valls et al. (2003) investigated the impact of eating a diet rich in corn oil with or without antioxidant supplementation of vitamin E (30 mg per day) on the antioxidant status and oxidative damage of AT in male Wistar rats. This study showed that the activity of the antioxidant enzymes CAT and SOD was reduced by taking a hyperlipidemia supplement along with vitamin E in AT [104].

In one study, Arias et al. (2014) examined the effect of quercetin (30 mg/kg body weight) in 28 male Wistar rats. This study shows that this supplement has no impact on reducing AT size and body weight. The activity of lipoprotein lipase and lipogenic enzymes remained unchanged with the use of this supplement [105]. Chen et al. (2020) investigated the effect of antioxidant supplementation of protease A-digested crude-chalaza hydrolysates (CCH-As) on Syrian male Golden Hamsters. They showed that adiposeperinatal/hepatic tissue size decreased as a result of consuming this antioxidant composition. Increased lipolysis (unpaired carnitine palmitoyltransferase 1, hormone-sensitive lipase, and protein 2) was also observed in these hamsters' AT [106]. Because mice, unlike humans, can endogenously synthesize vitamin C (ascorbate and ascorbic acid) and meet their daily needs, it is hypothesized that consuming extra amounts of vitamin C will counteract the anti-inflammatory effects. Therefore, in a study, researchers examined the effect of 4 weeks of vitamin C supplementation (low and high doses of 0.75 and 25 mg of ascorbic acid per kg of body weight, respectively) on male Wistar rats. Excessive consumption of this antioxidant supplement was able to strengthen antioxidant defenses (MnSOD, CuZnSOD, and CAT in AT [107]. Sung et al. (2012) investigated the effect of antioxidant supplementation of Polygonum aviculare L. (knotgrass) (PAE) in male C57BL/6J mice. They were given a high-fat diet or a high-fat diet with PAE antioxidant supplementation at a dose of 400 mg/kg body weight per day. In this article, the researchers found that adipose tissue weight, serum TG concentration, body weight, MDA and leptin concentrations, and fat cell area decreased as a result of taking this supplement [108]. Furthermore, Alcalá et al. (2015) examined the effect of taking antioxidant vitamin E supplementation (150 mg twice daily) in C57BL/6J mice. This study's results included a reduction in collagen deposition and OS in rat visceral AT. Consumption of this vitamin also led to increased storage capacity and fat cells' proliferation [30] (Table 1).


**Table 1.** The effect of antioxidant supplementation on obesity caused by oxidative stress (OS).
