Anticanbar Drugs

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

Main compounds of the enzymatic antioxidant system are three, namely, SOD, CAT and tT which have an important role in detoxifying of H2O2 and superoxide anion in cells. Ample of hepatotoxic drugs induces the liver damage by lipid peroxidation indirectly or directly. The proxy radicals are main factors that mediate lipid peroxidation leading to liver injury and kidney damage(41). MDA as a main reactive aldehyde appears during polyunsaturated fatty acid peroxidation in the biological

Your body is in a constant battle against infection, diseases and the formation of free radicals. However, there's a secret weapon that can help you fight against these things: antioxidants! Antioxidants are elements such as vitamins A, C and E that counteract the damage caused by free radicals and help protect your healthy cells. Free radicals are the molecules that contain unpaired electrons, which make them highly reactive. In this form, they can cause damage by attacking healthy cells, and when these cells grow weakened, you become more vulnerable to disease.

In the course of evolution man has lost his ability to produce some powerful antioxidants such as beta carotene and vitamin C in your body. Are preserved, however, other antioxidants (Eg melatonin) That inactivate free radicals and thus form a powerful defense system against them.

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

Pathogenesis of cardiac injury caused by doxorubicin is multifactorial and it is in direct relationship with metabolism and antitumor activity of the drug . Free radical stress, calcium overloading and mitochondrial dysfunction are main triggers in doxorubicin-induced cardiotoxicity. Subsequent gene expression changes and activation of the ubiquitin-proteasome system, cell death, as well as innate immunity activation all contribute to the toxicity (Shi et al., 2011). The level of the doxorubicin-induced oxidative stress is up to 10 times greater in the heart than in the other tissues (liver, kidney, spleen( Mukherjee et al., 2003) and therefore oxidative injury of the heart is widely accepted theory presumed as a primary mechanism of the DOX-induced cardiotoxicity. Formation of reactive oxygen species (ROS) has a leading role in promoting the oxidative myocardial

The ability of p53 to regulate metabolism is also associated with the ability to regulate cellular ROS levels. As previously mentioned, p53 can either remove damaged cells that have suffered sustained oxidative stress, or limit levels of ROS in order to lower oxidative stress and consequently, potential cell damage. Through the regulation of carbohydrate and lipid metabolism, p53 is able to influence the response to ROS accordingly. By driving the expression of TIGAR and promoting PPP activity, p53 can increase the production of NAPDH, which can be used to generate the cellular antioxidant GSH (Bensaad 2006). Moreover, at the expense of nucleotide synthesis, p53 can also promote GSH synthesis following serine starvation, thereby lowering ROS

As you may know, antioxidants promote good health as they help avoid diseases. More specifically, antioxidants help slow down the oxidation of cells in our body. When cells oxidize, they generate free radicals, which are also known as cellular bi-products. It is perfectly safe to have a manageable amount of these free radicals in the body. However, when the free radicals are in excess, they can wreak havoc on our organism's cellular

Metformin is one of the most widely prescribed antidiabetics for the type 2 diabetes. The critical role of metformin against tumorigenesis has recently been implicated, although several studies also reported the lack of anticancer property of the antidiabetics. Given the controversies regarding the potential role of metformin against tumour progression, the effect of metformin against breast, cervical and ovarian tumour cell lines was examined followed by in vivo assessment of metformin on tumour growth using xenograft breast cancer models. Significant The significant / A significant inhibitory impact of metformin was found on MCF-7, HeLa, and SKOV-3 cells, suggesting an antiproliferative property of metformin against breast, cervical and ovarian tumour cells, respectively, with the breast tumour cells, MCF-7, being the most responsiveness. in vivo assessment was carried out subsequently, where mice with breast tumours were treated with metformin (20 mg/kg bo. wt.) or sterile PBS solution for 15 consecutive days. No inhibition of breast tumour progression was detected in these rats. However, tumour necrosis was significantly increased in the metformin-treated group, accompanied by decreased capillary formation within the tumours.

Even though the MN is considered as surrogate measure of structural and numerical chromosomal aberrations, it is considered as a bridging biomarker of genotoxic exposure (Recioet al., 2010; Dertingeret al., 2007 ); and more importantly, it is indicative of increased cancer risk ( Bonassiet al., 2007 ). Certainly, the most reliable genotoxicity evaluation in mammals would be to combine chromosomal aberrations and micronuclei (Prasad et al., 2009). The MN assay in conjugation with CA, can give clues for both clastogenic damage and damage to the mitotic apparatus with aneugenic consequences and the MI (mitotic index)assay, is considereduseful method to characterize proliferating cells and identify compounds which inhibit or induce mitotic progression in mammalian system. More recently Eroglu (2010) showed MI as an effective measure to indicate the proportion of cells in the M–phase reflecting cellular death or delay in the cell proliferation kinetics.

Alteration in the antioxidant components like SOD and catalase, as noticed in this study has been linked to the cellular apoptotic signaling introduced by transcriptional factors and/or mitochondrial factors. The ratio of Bax/Bcl-2 in the high dose arsenic group (50mg/L) was significantly higher than that of the control group thus initiating apoptosis in liver and brain tissues [44]. Report reveals that inorganic arsenic-induced oxidative stress can cause cellular apoptosis in the cerebrum and cerebral locations [45]. These may be the reason behind the cerebrum and cerebellum tissue disarrangement and degeneration, in our present study. Green tea extract was found to be effiecient even in the restoration of the cellular morphology and tissue

They have the capacity to stay oxidize and help balance other molecules. Antioxidants have the remarkable ability to repair damaged molecules by donating hydrogen atoms to the molecules. The antioxidants neutralize the free radicals. Unfortunately, the antioxidants produced naturally by the body are not enough to neutralize all of the free radicals in the body. Therefore, a constant supply of external sources of antioxidants should be a part of one's daily diet, in order to reduce oxidative stress and related

VPA depletes cellular carnitine through the formation of valproylcarnitine and impairment of carnitine recycling in the mitochondria leading to inhibition of mitochondrial fatty acid oxidation (Lheureux et al., 2005). VPA inhibits biosynthesis of carnitine via inhibition of alpha-ketoglutarate. Carnitine supplementation increases beta-oxidation of VPA leading to reduction of cytoplasmic omega-oxidation and formation of toxic metabolites concerned in liver toxicity (Lheureux and Hantson, 2009). The beneficial effects of L carnitine appeared to be mediated via its strong antioxidant properties, which include the up regulation of the level of glutathione (Calabrese et al., 2006 and Thangasamy et al.,

CYP2E1 is a major cytochorme found to be involved in carbon-chlorine bond reductive cleavage and biotransformation of CCl4 to trichloromethyl radical (CCl3•). These cytochrome systems catalyze many reactions involved in drug metabolism and synthesis of cholesterol and other lipid metabolites both in endogenous substrates, such as ethanol and acetone as well as exogenous substrates which includes carbon tetrachloride (Tang et al., 2013). In the presence of oxygen, CCl3• generates the highly reactive metabolites such as trichloromethyl peroxy (CCl3OO•) free radicals which covalently bind to the cellular macromolecules, lipids and polyunsaturated fatty acids in the cellular membrane. Trichloromethyl peroxy (CCl3OO•) free radicals react with suitable substrates to complete its electron pair. CCl3OO• is

Numerous scientific studies show that the people whose food intake is rich in antioxidants and who also take antioxidant supplements, have better chances to live longer, healthier and happier lives. Antioxidants are a family of vitamins, minerals, and other nutrients that may prevent or delay some types of cell damage. Thus, they might be beneficial in preventing diseases and contribute to the length and quality of human life. Hundreds of antioxidants are produced in the human body, but some necessary antioxidants must be obtained from the outer sources. But do they work separately in our bodies? Or antioxidants in our bodies can incorporate with each other in order to improve human lives. Some studies about antioxidants come up with a