Superoxide Dismutase Research Paper

Catalase is an important enzyme that protects cells from oxidative damage, which hydrogen peroxide can cause. It is an incredibly efficient enzyme where one catalase molecule can convert millions of hydrogen peroxide molecules each second.

Compared to diabetic control rats, total antioxidant levels were significantly increased in GTE supplemented rats. Inversely, malondialdehyde levels and AT(1) receptor were significantly lower in the GTE supplemented diabetic group [77]. Catechin and its derivatives in green tea are shown to be therapeutically very effective.

Peroxynitrite (ONOO−) is a well known potent oxidant and nitrating agent that is formed through the interaction of (NO•) with superoxide ion (O2•-) and its production is allied to the superoxide sources (for instance mitochondrial respiratory complexes or NAD(P)H oxidases present on plasma membrane) because superoxide is a shorter lived species and also shows constrained diffusion across biological membranes whereas NO• is quite stable and extremely diffusible free radical. In vivo, the rate of production in particular organelles (such as phagocytic vacuoles in macrophages) is very high as 50–100 μM per min. The ability of peroxynitrite to cross cell membranes despite of having short half-life at physiological pH (~10 ms) suggested that peroxynitrite formed could persuade adjoining target cells within one to two cell diameters (~5–20 μm) (Denicola et al., 1998). The decomposition of peroxynitrite occur via proton-catalyzed manner to form OH• and NO2• radicals in hydrophobic phases and initiates lipid peroxidation (Radi et al., 1991; Bartesaghi et al., 2006).

This indicates that the metabolism of proteins was apparently affected by Ch.t extract. The improvement on the levels of protein and albumin in the diabetic treated groups show that Ch.t extract have significant effect in glucose and protein level because insulin inhibit gluconeogenesis from protein [ ] or could be due to improvement in renal function. This affirmative agrees with the fact that the weight of skeletal muscles was significantly increase in diabetic rats treated with Ch.t extract. The decrease in albumin level documented for diabetic rats may be due to liver massive necrosis, deterioration of liver function, hepatic resistance to insulin and glycogen impairment of oxidative phosphorylation[ ].Under the same experimental conditions serum globulin level revealed an appreciable decrease[ ]. The renal pathogenesis is related to duration of diabetes, the most devastating complication with diabetes is nephropathy[

With all living organisms, a process known as cell respiration is integral in order to provide the body with an essential form of energy, adenosine triphosphate (ATP). Oxygen, although an essential part of this process, can form reactants from colliding with electrons associated with carrier molecules. (pb101.rcsb.org, 2017). Hydrogen peroxide is an integral product of this reaction but is known to impose negative effects on the body if high levels are introduced. Explicitly, this reaction is caused “If oxygen runs into (one of these) carrier molecules, the electron may be accidentally transferred to it. This converts oxygen into dangerous compounds such as superoxide radicals and hydrogen peroxide, which can attack the delicate sulphur atoms and metal ions in proteins.” (pdbh101.rcb.org, 2017). Research has suggested that the hydrogen peroxide can be converted into hydroxyl radicals, known to mutate DNA, which can potentially cause bodily harm due to DNA’s role in the synthesis of proteins. These radicals can cause detrimental effects on the human body, and studies have suggested a link to ageing. Due to the harmful effects of these H2o2, it is important that the body finds a way to dispose of hydrogen peroxide before concentrations are too great.

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

Several possible mechanisms have been explained regarding diabetes induced neurodegeneration. Diabetes mellitus and the accompanying hyperglycemia is a chronic endogenous stressor that is accompanied with increased oxidative stress in brain, particularly the hippocampus, by accelerating free radical generation. These radicals contribute to increased neuronal degeneration by inducing oxidation to proteins, DNA alterations and lipids oxidation in cell membranes .

These superoxides may be dangerous because they alter the structure of iron and protein via reduction. They may also undergo dismutation to form hydrogen peroxide which, in turn, gives rise to hydroxyl radicals, the most reactive ROS (Gulumian and Van Wyk, 1987; Agarwal et al., 2005). Hydrogen peroxide is not a free radical but its neutral charge allows it to pass through cell membranes and so this makes it very dangerous (Kurutas, 2015). Other internal or endogenous sources for these free radicals are inflammation, xanthine oxidase, peroxisomes, phagocytosis, exercise and ischaemia. Exogenous factors which lead to the development of these ROS include smoking, ozone, environmental pollutants, radiation, pesticides and drugs (Lobo et al.,

The roles of antioxidants( Endogenous compounds) are to neutralize the excess of free radicals, to protect the cells against their toxic effects and to contribute in disease

Superoxide dismutase 1 is the most commonly ALS aggregated protein to be identified since its discovery over two decades ago (Rosen et al., 1993; Tortelli et al., 2013). SOD1 is a 153 amino acid homodimer with a copper-zinc active site (Brotherton et al., 2013; Dangoumau et al., 2014). Mutant SOD1 is responsible for the loss of motor neurons and constitutes an estimated 20% of the familial ALS (fALS) cases (Brotherton et al., 2013; Tortelli et al., 2013). Wild type SOD1 is universally expressed in all cells and is responsible for the removal of free radicals often in the form of reactive oxygen species (ROS) (Brotherton et al., 2013; Chiang et al., 2017). Damage to DNA and degradation to metabolic processes occur due to accumulation of ROS

Xanthine oxidase is a form of xanthine oxidoreductase, a type of enzyme generating ROS [7]. Xanthine oxidase varies widely in abundance among cell types, organs and species, and its involvement in reperfusion injury depends on its ability to produce superoxide. As is shown in Figure 1, this enzyme catalyzes the oxidation of hypoxanthine to xanthine and can further catalyze the oxidation of xanthine to uric acid, producing hydrogen peroxide [8]. Under some circumstances, it can produce

The intracellular redox state is a dynamic system which may modify on many factors. Mitochondria are essential to sustain life and the main intracellular source for fuel generation; moreover engaged in the regulation of many intracellular functions such as redox homeostasis and cell fate. The mitochondrial dynamics have changed and reactive oxygen species (ROS) generation could encourage the induction of oxidative DNA damage, inactivation of phosphatases and transcription factors. Moreover the mitochondrial dysfunction may constantly accompanied and contributed for a broad range of human diseases. Mitochondrial disrepair will result in oxidative stress, which is one of the underlying causal factors for a variety of diseases. High levels of

The role of oxidative stress is the imbalance of detoxified free radicals. When the body fails to detoxify free radicals, the free radicals take an electron from another molecule. As a result, the molecule is no longer stable. An unstable molecule can lead to damage within the cell and cause the cell to function improperly. Therefore, preventing oxidative stress is very important for the cell to maintain its proper function. If the cell does not function properly, an increase in antioxidants can help to repair the cell. Antioxidants are produced by the cell but increasing antioxidants for example in ones diet can reduce the amount of free radicals in the body that cause harm and as a result lead to oxidative stress in the body.

Meta-analyses showed that zinc supplementation has a favorable effect on glycemic control in diabetic patients (260). Furthermore, zinc supplementation in diabetic mice and rats significantly reduce diabetes-induced renal damage (261). In STZ-induced diabetic rats, zinc supplementation can attenuate diabetes-induced renal pathological changes likely through prevention of hyperglycemia-induced CTGF expression by zinc -induced cardiac metallothionein in renal tubular cells (262). It was found also that supplementation of zinc improved the effectiveness of hypoglycemic agents and may be beneficial in decreasing BSL, triglyceride, urinary albumin excretion and inflammation in type 2 diabetic nephropathy patients (263). Recent study showed that zinc has a protective effect against diabetic damage through stimulation of metallothionein synthesis, a potent antioxidant, and regulation of the OS

Dill (Anethum graveolans L.) aerial parts a renewed interest in medicinal plants because generally they do not elicit any side effects. In present study, effect of the hydro-alcoholic extract of the Anethum graveolans L. aerial parts on serum glucose, total cholesterol, triglyceride, C-LDL, C-HDL, urea, uric acid, creatinine, alkaline phosphatase (AP), alanine aminotransaminase (ALT) and aspartate aminotransaminase (AST) enzymes levels were investigated in alloxan-induced diabetic rats. The animals were made diabetic using by alloxan (90 mg/kg, i.p.). The hydroethanolic extract at doses 50, 100, 200 and 300 mg/kg, i.p. were administered for 14 days, intraperitoneally. Blood samples were obtained from heart after 14 days. The group of