A Brief Overview of Oxidative Stress in Adipose Tissue with a Therapeutic Approach to Taking Antioxidant Supplements

Abstract

One of the leading causes of obesity associated with oxidative stress (OS) is excessive consumption of nutrients, especially fast-foods, and a sedentary lifestyle, characterized by the ample accumulation of lipid in adipose tissue (AT). When the body needs energy, the lipid is broken down into glycerol (G) and free fatty acids (FFA) during the lipolysis process and transferred to various tissues in the body. Materials secreted from AT, especially adipocytokines (interleukin (IL)-1β, IL-6, and tumor necrosis factor-α (TNF-α)) and reactive oxygen species (ROS), are impressive in causing inflammation and OS of AT. There are several ways to improve obesity, but researchers have highly regarded the use of antioxidant supplements due to their neutralizing properties in removing ROS. In this review, we have examined the AT response to OS to antioxidant supplements focusing on animal studies. The results are inconsistent due to differences in the study duration and diversity in animals (strain, age, and sex). Therefore, there is a need for different studies, especially in humans.

Cardiac Oxidative Stress and the Therapeutic Approaches to the Intake of Antioxidant Supplements and Physical Activity

“…The cytosolic enzyme GPx catalyzes the dismutation of H 2 O 2 into oxygen and water and even the conversion of peroxide radicals to alcohols and oxygen [33]. To date, there are eight different isoforms of GPx [1][2][3][4][5][6][7][8], with GPx-1 being the most common isoform found in the cytoplasm of all mammalian cells. Glutathione peroxidase 1, a ONOO − reductase enzyme prevalent throughout most cells, such as the endothelium, converts H 2 O 2 to water and lipid peroxides to their corresponding alcohols using glutathione [27,34].…”

“…Reactive oxygen species (ROS) are cellular metabolic byproducts that are biologically produced and cause oxidative stress [1]. In addition, ROS contain oxygen that is regulated by antioxidant defense systems that are both non-enzymatic and enzymatic [2,3]. ROS modulate cell growth, and heart excitation-contraction coupling and play an integral part in cellular processes, and are useful in modulating processes involved in the maintenance of homeostasis and diverse cellular activities at low-to-moderate levels [2,4].…”

The Role of NRF2 in Obesity-Associated Cardiovascular Risk Factors

“…The development of CVD is intimately linked to the pathogenesis of obesity, which includes an increase in the levels of circulating free fatty acid (FFA; including palmitate), ROS and reactive nitrogen species (RNS), causing chronic inflammation, which is another important source of oxidative stress, and insulin resistance [ 16 , 18 ]. Regarding oxidative stress, BMI is positively associated to indicators of protein, lipid, and DNA oxidative damage (advanced oxidation protein products (AOPP), malondialdehyde (MDA) or 8-iso-prostaglandin F2α (8-iso-PGF2α), and 8-hydroxy-2′-deoxyguanosine (8-OHdG) during obesity (reviewed in [ 44 ]). Moreover, epicardial fat is a source of ROS and inflammatory status, which are closely linked to obesity-related cardiac dysfunction [ 45 , 46 ].…”

An Overview of Physical Exercise and Antioxidant Supplementation Influences on Skeletal Muscle Oxidative Stress

“…Approximately five distinct NOX protein homologues have been expressed and detected in various tissues of the body. For example, NOX2 is expressed in SM and is the predominant source of ROS generation in both contractile and resting states [24,25]. Furthermore, this enzyme accelerates the oxidation of the ryanodine receptor (RyR) and the interruption of calcium release by the sarcoplasmic reticulum (SR), resulting in SM contraction failure [26].…”