Oxidative Stress (T2DM)

Type 2 diabetes mellitus (T2D) is the most common form of diabetes (American Diabetes Association, 2012). T2D is so prevalent that it is estimated to be the fifth most common cause of death worldwide (Yates, Jarvis, Troughton, and JaneDavies, 2009, p. 1). T2D manifests when the body is unable to metabolize glucose properly, resulting in elevated blood sugar, debilitating fatigue, and other serious complications such as distal limb amputations, kidney failure, and blindness. The generally accepted causes of T2D include diet, sedentary lifestyle, and obesity.

Diabetes is a growing concern and health challenge for the American people (b). Diabetes is a condition in which the body cannot react to insulin appropriately or either cannot produce insulin efficiently (w). “Without a properly functioning insulin signaling system, blood glucose levels become elevated and other metabolic abnormalities occur, leading to the development of serious, disabling complications” (w). There are numerous forms of diabetes amongst the nation, however, there are three main forms of diabetes. Most people have heard of type one diabetes, type two diabetes, and gestational diabetes because they are common. Type two diabetes deals with a resistance to insulin, while

Superoxide dismutase (SOD) is a free radical scavenging enzyme that catalyses the dismutation of highly reactive superoxide anion O2 to molecular (O2) and to the less reactive species hydrogen peroxide. It has been proposed that poor glycemic control in diabetes is associated with depletion of antioxidant enzymes including SOD.

Type 2 diabetes is a polygenic, complex disease that has become a worldwide health crisis. According to the World Health Organization over 422 million people in the world had this disease in 2014 (1), the Center for Disease Control and Prevention stated that in the United States alone 29 million people had diabetes in 2014 (2). While the genetic predisposition contributing to the diabetes phenotype is not fully understood to date it still remains an area of active research. There are also various environmental factors that contribute stress to the glucose homeostasis system that provide a different approach in understanding this disease. Comprehending the pathogenesis of the disease has been an area of constant research for decades. There is hope that pharmaceutical developments can follow along and find medical treatments that can target the key pathogenic elements of this disease.

"Conditions such as muscle pain or skin irritation were associated with low serum levels of selenium or zinc." (Wichert et al.) "Deficiencies may cause hair loss and poor wound healing." "Low intakes of selenium cause white muscle disease. Foals are born weak and may not be able

Similarly, an increase in the levels of lipid peroxidation was observed in Aβ-induced rat hippocampal cells, confirming previous reports [17]. Enzymatic antioxidants such as SOD, catalase, and GPX act as the cellular antioxidant defense mechanism against free radicals. Since NADPH is required for the regeneration of catalase from its inactive form, catalase activity might be decreased in Aβ induced toxicity due to reduced NADPH levels. In this study, we have reported that Honokiol treatment significantly increased the enzymatic antioxidant activities in APP-CHO cells. In addition, non-enzymatic antioxidants like GSH also exhibited beneficial neuroprotective effects against oxidative stress. GSH is an endogenous nonenzymatic antioxidant that prevents damage to cellular components caused by ROS such as free radicals and peroxides. GSH is oxidized to glutathione disulfide (GSSG) by ROS, thereby causing a reduction in the level of GSH. GR reduces GSSG to GSH via NADPH, which in turn is released by glucose-6-phosphate dehydrogenase [18]. Honokiol treatment upregulated the activity of these antioxidants in APP-CHO cells. In addition to oxidative stress, a strong association between insulin resistance and the development of AD has been demonstrated. Several studies have reported that insulin resistance (IR), an underlying characteristic of type 2 diabetes, is an important risk factor for AD

Selenium is an essential trace element found in the body that works in conjunction with other vitamins to support the powerful detoxification process. When combined with Vitamin E, Selenium can help prevent oxidative stress from occurring in the body which is crucial in the prevention of many diseases such as heart disease and cancer. According to Dr. Mandal (2015), "Oxidative stress is essentially an imbalance between the production of free radicals and the ability of the body to counteract or detoxify their harmful effects through neutralization by antioxidants." Selenium goes to work in the body as a powerful antioxidant, and it is required for the production of Glutathione, which is a key antioxidant in our bodies. Antioxidants are important in keeping the body healthy by fighting off the free radicals that our cells are exposed to on a daily basis.

in todays world people being busy in their work fitness life family friends technology many more they are shifting from not taking proper care of themselves. becoming fit is not the solution. there are many infirmities related to body cell which can cause loss of happiness wealth etc. diseases can be caused because of microbes unclean environment pathogens etc. but some diseases or infirmities occurs due to various changes inside the body. these changes are chemical changes and one such change is oxidative stress occurring in the body; inside the cells and its consequences could be acute as well as chronic. oxidative stress is defined as the imbalance between the reactive oxygen species the biological systems to reduce or detoxify the reactive

Diabetes mellitus (DM) is one of the major problems in health system and a worldwide general health risk that has increased drastically in the course of recent decades (1, 2). As per epidemiological studies, the number of patients with DM expanded from around 30 million cases in 1985, 177 million in 2000, 285 million in 2010, and evaluated if the circumstance continues with the same , more than 360 million individuals by 2030 will have DM (3).

Module ten discussed oxidative stress, and the causes, as well as consequences of liver disorders. Oxidative stress occurs when there is an abnormal balance between nonspecific oxidation reactions, and the body's ability to counteract them. A nonspecific oxidation reaction refers to one that involves free radicals reacting in a disorderly fashion with other molecules. Free radicals are highly reactive molecules that can cause cellular damage, targeting that of carbohydrates, lipids, proteins and nucleic acids. Free radicals within the body can lead to fragmentation of proteins causing them to have an abnormal function, oxidize polysaturated lipids at their double bond causing disruption in the membrane function, and cause mutations in DNA. Antioxidants react directly with free radicals in the body to render them inactive. Some antioxidant

Enhanced oxidative stress and changes in antioxidant capacity, found in both clinical and experimental diabetes, are thought

Oxidative stress is widely accepted to be associated with dysfunction of pancreatic β-cells as well as insulin resistance in type 2 diabetes (Henriksen et al., 2011). Experimental evidences suggest the involvement of free radicals in the onset of diabetes and more importantly in the development of diabetic complications (Lipinsky, 2001). Studies have revealed decreases in expression of genes for antioxidant enzymes, such as superoxide dismutase (SOD), glutathione peroxidase, and catalase in diabetic models (Lenzen et al., 1996). Also a decrease in the activities of the antioxidant/ antioxidant enzyme systems in diabetics are linked to the progressive glycation of the enzyme proteins (Hartnet et al., 2000). The interrelationship between the antioxidative potentials and antidiabetic activities of bioactive compounds is still unclear. In the present study, the extent of free radical damage orchestrated by STZ administration was significantly reduced by the antioxidant composition and combination treatment in a dose-dependent manner; thereby reducing the extent of pancreatic β-cell damages among the rats co-treated with combination therapy and STZ, relative to normal and STZ-only rats. The HFD/STZ-induced diabetic control rats had significantly lower (p< 0.05) of total SOD, CAT, GST and GPx activities among the extracts, cell gevity, antioxidant composition and combination therapy co-treated rats (Figure 4.2.34, Figure 4.2.35, Figure 4.2.36, Figure 4.2.37). HFD/STZ decreased the

During physical activity, the body undergoes many changes in the muscles, lungs, heart, and bones. The heart rate increases as the activity level increases, this happens to supply more oxygenated blood to the muscles. When there is an increase in training it decreases the resting heart rate, and the blood pressure decreases due to blood vessel formation (Larson et al. 2012). An individual who may use this to supplement their physical activity would be someone most likely trying to avoid disease. For instance, in stage 1 hypertension, unhealthy, or has an obese gene. Sustained high blood pressure can result in hypertension which is a precursor to the development of cardiac and/or renal hypertrophy (Duarte et al. 2001). Seen in prior animal studies and in Edwards et al. (2007) the patient must be at a specific range (over 120/80 mm Hg) in order for quercetin supplementation to show effects.

SelW expression it has been found to work as regulated during C2C12 cell differentiation (Noh et al 2010). The mRNA level of SelW through the differentiation process of myoblasts and the optimal Se concentrations for expression of SelW mRNA in chicken myoblasts is 10−7 M is influenced by Se( Ruan et al 2012.) Overexpression of SEPW could decrease the H2O2- influence oxidative damage.furthermore, the increased expression of certain antioxidative selenoproteins could regulate oxidation–reduction homeostasis in cells, improve the ability of cells to save against oxidative stress and reduce the oxidative damage and the concentration of H2O2 (Yao et al 2014). overexpression of SelW experiment indicated that it might play important role in component of the cellular defense system against oxidative stress (Sun et al., 2001) . Increased of Malondialdehyde (MDA) levels found to be induced with SEPW1 deficiency , also It is reported that Sepw1 deficiency reduced the ability of myoblasts to buffer the exogenous H2O2 and increased the sensitivity of cells to H2O2. Therefore, Sepw1 plays beneficial role in antioxidative functions in myoblasts also indicating that Sepw1 and Gpx1 may play important roles in the response to oxidative stress in chicken myoblasts. Therefore, chicken Sepw1 also preserves antioxidative function (Yao et al 2014).

Effects of DL- 2-hydroxy-4(methylthio)butanoic acid supplementation on antioxidant capacity and its related gene expression in lung and liver of broilers exposed to low temperature