Essay On Bacocosides

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.

As well as this, Nox2 affects the level of HIF-2a, which is responsible for anti-oxidative activity, and decreases it that lead to increased oxidative responses and neuronal

Treating cells with 0.1mg/ml of 200W sonicated pectin led to 82.82% viable cells, 3.95% early apoptotic cells and 9.84% late apoptotic cells, and according to Fig. 5e, treatment with 0.5mg/ml of 200W sonicated pectin led to reduction of viable cells 56.09%, early apoptosis increased to 14.32 and late apoptosis was 25.18%. The differences between untreated cells and treated cells were all significant (p < 0.05). From the results induction of apoptosis could be linked to pectin concentration, neutral sugar composition, galacturonic acid content and molecular weight, with low molecular weight pectin seemingly more potent than low molecular weight and the higher galactose and galacturonic acid content the higher the activity. The 400W treated pectin had low molecular weight and higher proportion of galactose compared to 200W sonicated

Under normal condition, ROS production in the brain is balanced by the endogenous enzymatic and non-enzymatic anti-oxidative mechanisms. The enzymes include superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase. SOD catalyzes dismutation of superoxide to hydrogen peroxide, providing the first line against ROS damage [46, 70]. GPX and catalase further metabolize hydrogen peroxide to water and oxygen [71]. In the process, reduced glutathione (GSH) is oxidized to oxidized glutathione (GSSG) and it can be recycled by the NADPH-dependent GSSG reductase [72]. Non-enzymatic endogenous anti-oxidative small molecules also play very important roles in defending against oxidative stress, especially in extracellular space that the enzymes are absent or in very low levels [73]. Small-molecule anti-oxidant can be water-soluble or lipid-soluble, these molecules include glutathione, vitamin E and C (inhibits

Oxidative stress and inflammation play a causative role in epileptogenesis and ictogenesis by taking part in neurodegeneration and excite-toxic neuronal injury (4-6). On the other hand, prolonged seizures lead to neuronal cell death by inducing mitochondrial dysfunction and incre-asing reactive oxygen species (ROS) and nitric oxide (NO). Moreover, ROS may prolong gluta-mate presence at synapses and result in further neurotoxicity (7).

Oxidants will affect mitochondrial redox status and may cause extensive oxidative damage to proteins(Kalyanaraman et al .,2002). Furthermore, the mitochondrial transition pore can open releasing cytochrome c and possibly affecting mitochondrial function. Cytochrome c can activate cytosolic caspases to induce apoptosis. Doxorubicin may induce anti-apoptotic (Bcl-2, Bcl-XL) and pro-apoptotic (Bax, Bad) proteins. The Bcl-2 family of proteins regulates the release of cytochrome c . These include Bax, Bad, and Bid, which are pro-apoptotic proteins that favor cytochrome c release and Bcl-2 and Bcl-XL which are anti-apoptotic proteins that inhibit cytochrome c release . The mechanisms of how Bcl-2 family proteins regulate release of cytochrome c and apoptogenic factors are under investigation.

The hypoxia-inducible factor prolyl hydroxylase domain enzymes (HIF-PHDs) are a family of oxygen sensors that has been implicated in neuronal survival. Catalysis by the HIF-PHDs destabilizes the transcriptional activator HIF-1a under normoxia. HIF-PHDs are promising target candidates for mitochondrial protection in paradigms of oxidative stress. The inhibition of HIF-PHDs prevented neuronal cell death induced by mitochondrial toxins [1][2].

[98, 99]. The detrimental effects of ROS become more pronounced with age due to the limits of cellular antioxidant defense systems.

Damage to proteins and lipids as well as DNA has been shown to increase during aging in numerous organisms comprise of Caenorhabditis elegans, Drosophila melanogaster, mice, rat and humans. (Golden et al. 2002; Hamilton et al. 2001; Sohal et al. 1993; Stadtman 2001; Yan&Sohal 1998). Reduction in antioxidant defense system or significant increment in oxidative stress has resulted in poor lifespan (Ishii et al. 1998; Melov et al. 1999; Moskovitz et al. 2001). With a growing body of evidences towards the oxidative stress theory, an exact relationship between accumulation of reactive species or oxidative stress theory and aging process especially cognitive deterioration has not yet been establish and strongly proven. Therefore, understanding the mechanisms of cognitive decline is likely to be important in developing effectiveness intervention for a better

An increase of peroxidase activity is one of the key points, which contributes to the mitochondrial synthesis of reactive oxygen species (ROS) for example CL oxidation. Since ROSs are normally regarded as harmful factors to the cell, the increase level of ROS has a significant role in inducing apoptosis. Thus, the oxidation of CL might be necessary to induce the mitochondria membrane leakage, and release of pro-apoptotic substances, such as protein tyrosine phosphatases (PTP) into the cytosol.Additionally, the released cyt c can play some other roles. It can interact with and oxidize another phospholipid phosphatidylserine (PS) with negative charges, which is another important function of cyt c in apoptosis.12 It is also able to bind to the apoptotic protease-activation factor-1 (APAF1), and stimulate its heptamerization to finally activate the caspase based apoptosis.13 Lots of detailed studies have been done on the cyt c-lipid interaction which will be discussed later in the

Oxidative stress has been implicated in various pathophysiological conditions either directly or indirectly. They are cardiovascular disease, cancer (1), neurodegenerative diseases such as Parkinson’s disease (PD), Alzheimer’s diseases (AD) (2,3), Amyotrophic lateral sclerosis (ALS), Huntington’s disease, and multiple sclerosis, Diabetes Mellitus (4), ischemia/reperfusion, fibrosis, Kidney disease, impairment via cochlear damage induced by elevated sound levels, ototoxicity of drugs such as cisplatin, and in congenital deafness in both animals and humans, obstructive sleep apnea, obesity, hypertension, diseases of prematurely and other diseases related to ageing (5). These diseases fall into two groups.

Malondialdehyde is produced from decomposition of products of lipid peroxidation (Gaweł et al., 2004). Thus, the observed increased MDA levels may arise from the attack of the neuronal membrane phospholipids by free radicals produced from monoamine catabolism. In addition, the

Oligodendrocytes are the most vulnerable brain cells to oxidative stress due to its high metabolic demand for synthesizing myelin sheaths (Ichinose et al., 2014), and relatively low levels of antioxidants (Lassmann and Van Horssen, 2011). Accumulating evidence suggests that oxidative stress plays a major role in the pathogenesis of MS. In the present study, cuprizone diet significantly increased brain TBARS level and decreased GSH content. These results are consistent with previous reports which reported that reactive oxygen species (ROS), produced as a consequence of alteration in the mitochondrial electron transport chain, have been implicated as mediators of demyelination and axonal damage in both MS and its animal models (Ghaiad et al., 2017; Kashani et al., 2014). On the other hand, treatment with linagliptin showed significant reduction in TBARS level and increase in GSH

For the treatment of many diseases, particularly cancer, substantial attention is presently focused on the use of drugs without side effects and to study the underlying mechanisms of their actions. Precisely, the action of endogenous enzymatic antioxidants capable of eliminating the oxidants and free radicals accountable for cancer initiation and progression, have been extensively debated [27]. Molecular uncovering of the antioxidant physiognomies of different anticancer drugs in addition to food and environmental substantces have been implemented [28]. Cellular antioxidantive enzymes have been inspected for their role in inhibition of diseases such as cancer, coronary heart disease and also altitude sickness [29]. The antioxidant

The reactivity of HOCl has been comprehensively assessed with in a wide range of cellular systems, including yeast (Carmona-Gutierrez et al., 2013) and bacteria (Winterbourne and Kettle, 2013; Winterbourne et al., 2006; Chapman et al., 2002), together with many studies focused on specific mammalian cell types and tissues. It is clear from the numerous invitro studies that HOCl is highly reactive and destructive, inducing cell death via both necrotic and programmed apoptotic pathways, depending on the oxidant concentration and cell type under study.