scholarly journals Amelioration of Isoproterenol-Induced Oxidative Damage in Rat Myocardium byWithania somniferaLeaf Extract

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Md. Ibrahim Khalil ◽  
Istiyak Ahmmed ◽  
Romana Ahmed ◽  
E. M. Tanvir ◽  
Rizwana Afroz ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Troponin I ◽  
Protective Role ◽  
Lipid Profiles ◽  
Enzymatic Antioxidants ◽  
Marker Enzymes ◽  
Glutathione S Transferase ◽  
Myocardial Membrane ◽  
Endogenous Antioxidant

We investigated the protective role ofWithania somniferaleaf extract (WSLEt) on isoproterenol- (ISO-) induced myocardial infarction (MI) in rats. Subcutaneous injection of ISO (85 mg/kg body weight (b.w.)) administered to rats for two consecutive days caused a significant increase in cardiac troponin I (cTnI) levels and serum lipid profiles, as well as the activities of some marker enzymes. In addition to these diagnostic markers, there were increased levels of lipid peroxidation (LPO) and decreased activities of enzymatic antioxidants (superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GRx), and glutathione-S-transferase (GST)) in the myocardium. However, oral pretreatment (100 mg/kg b.w.) with WSLEt for 4 weeks elicited a significant cardioprotective activity by lowering the levels of cTnI, lipid profiles, and marker enzymes. The levels of LPO products were also significantly decreased. Elevated activities of antioxidant enzymes were also observed in rats pretreated with WSLEt. As further confirmed histopathologically, our findings strongly suggest that the cardioprotective effect of WSLEt on myocardium experiencing ISO-induced oxidative damage may be due to an augmentation of the endogenous antioxidant system and an inhibition of LPO in the myocardial membrane. We conclude that WSLEt confers some protection against oxidative damage in ISO-induced MI in rats.

scholarly journals Dietary quercetin abrogates hepatorenal oxidative damage associated with dichloromethane exposure in rats

2019 ◽  
Author(s):  
Solomon E Owumi ◽  
Olabisi F Danso ◽  
Magdalene E Effiong
Keyword(s):  
Oxidative Damage ◽  
Protective Role ◽  
Gamma Glutamyl Transferase ◽  
Glutathione S Transferase ◽  
Histological Changes ◽  
Chlorinated Solvent ◽  
Household Products ◽  
Liver And Kidney ◽  
Glutamyl Transferase

Exposure to dichloromethane (DCM), a commonly used chlorinated solvent in industrial settings and for the production of many household products, reportedly elicits detrimental effects in animals and humans. The present study investigated the protective role of dietary quercetin on DCM-induced hepatorenal damage in rats. Experimental rats were orally administered with DCM (150 mg/kg) and 30 min later with quercetin at 10, 20 and 40 mg/kg or none for 7 consecutive days. The results indicated that DCM-mediated significant (p<0.05) increases in serum alanine aminotransferase, aspartate aminotransferase, gamma glutamyl transferase and alkaline phosphatase activities as well as urea and creatinine levels were dose-dependently normalized to the control values in rats co-treated with quercetin. Further, quercetin co-treatment ameliorated DCM-mediated decrease in the hepatic and renal activities of superoxide dismutase, catalase, glutathione peroxidase and glutathione S-transferase as well as glutathione level in the treated rats. Moreover, quercetin co-treatment markedly reduced lipid peroxidation level and protected against histological changes in liver and kidney of the treated rats. Taken together, quercetin abrogated hepatorenal oxidative damage in DCM-treated rats via improvement of antioxidant status and suppression of oxidative damage.

The protective role of ferulic acid on sepsis-induced oxidative damage in Wistar albino rats

2014 ◽  
Vol 38 (3) ◽  
pp. 774-782 ◽  
Author(s):  
Merve Bacanlı ◽  
Sevtap Aydın ◽  
Gökçe Taner ◽  
Hatice Gül Göktaş ◽  
Tolga Şahin ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Ferulic Acid ◽  
Protective Role ◽  
Albino Rats ◽  
Wistar Albino Rats

NADPH oxidase participates in the oxidative damage caused by fluoride in rat spermatozoa. Protective role of α-tocopherol

2010 ◽  
Vol 31 (6) ◽  
pp. 579-588 ◽  
Author(s):  
Jeannett A. Izquierdo-Vega ◽  
Manuel Sánchez-Gutiérrez ◽  
Luz María Del Razo
Keyword(s):  
Oxidative Damage ◽  
Nadph Oxidase ◽  
Protective Role

scholarly journals Ameliorative Effects of Honey, Propolis, Pollen, and Royal Jelly Mixture against Chronic Toxicity of Sumithion Insecticide in White Albino Rats

Molecules ◽  
2020 ◽  
Vol 25 (11) ◽  
pp. 2633 ◽  
Author(s):  
Atef M.K. Nassar ◽  
Yehia M.M. Salim ◽  
Khalid S.A. Eid ◽  
Hazem M. Shaheen ◽  
Abdullah A. Saati ◽  
...  
Keyword(s):  
Royal Jelly ◽  
Corn Oil ◽  
Ethylenediaminetetraacetic Acid ◽  
Reproductive Organs ◽  
Protective Role ◽  
Albino Rats ◽  
Total Protein Content ◽  
Glutathione S Transferase ◽  
Significant Toxicity

Sumithion (Fenitrothion) (SUM) is an organophosphorus insecticide used to combat a wide variety of plant pests. Exposure to SUM causes significant toxicity to the brain, liver, kidney, and reproductive organs through, for example, binding to DNA, and it induces DNA damage, which ends with oxidative stress. Therefore, the present study aimed to examine the protective role of bee products: a mixture of honey, propolis, palm pollen, and royal jelly (HPPJ) against SUM-induced toxicity. Twenty-four male albino rats (Rattus norvegicus) were classified into four groups, each containing six rats: control (corn oil), SUM (85 mg/kg; 1/20 LD50), HPPJ, and SUM + HPPJ once daily for 28 consecutive days. Blood samples were gently collected in sterilized ethylenediaminetetraacetic acid (EDTA) tubes for blood picture analyses and tubes without anticoagulant for serum isolation. Serum was used for assays of enzymatic and biochemical characteristics. The results revealed that SUM increased the weights of the liver, kidney, and brain as well as the enzymatic activity of glutathione peroxidase (GP), serum superoxide dismutase (SOD), and glutathione-S-transferase (GST). Additionally, SUM significantly increased the activity of lactate dehydrogenase (LDH), alkaline phosphatase (ALP), and γ-glutamyltransferase (γ-GT) and glucose, uric acid, and creatinine contents, while decreasing the acetylcholine esterase (AChE) activity and total lipids and total protein content. Furthermore, because of the inclusion of phenolic, flavonoids, terpenoids, and sugars, the HPPJ mixture counteracted the hematological, renal, and hepatic toxicity of SUM exposure.

scholarly journals Mapping hole hopping escape routes in proteins

2019 ◽  
Vol 116 (32) ◽  
pp. 15811-15816 ◽  
Author(s):  
Ruijie D. Teo ◽  
Ruobing Wang ◽  
Elizabeth R. Smithwick ◽  
Agostino Migliore ◽  
Michael J. Therien ◽  
...  
Keyword(s):  
Oxidative Damage ◽  
Protective Role ◽  
Residence Times ◽  
P450 Monooxygenase ◽  
Protection Mechanism ◽  
Biologically Relevant ◽  
Redox Active ◽  
Catalytic Sites ◽  
Benzylsuccinate Synthase

A recently proposed oxidative damage protection mechanism in proteins relies on hole hopping escape routes formed by redox-active amino acids. We present a computational tool to identify the dominant charge hopping pathways through these residues based on the mean residence times of the transferring charge along these hopping pathways. The residence times are estimated by combining a kinetic model with well-known rate expressions for the charge-transfer steps in the pathways. We identify the most rapid hole hopping escape routes in cytochrome P450 monooxygenase, cytochrome c peroxidase, and benzylsuccinate synthase (BSS). This theoretical analysis supports the existence of hole hopping chains as a mechanism capable of providing hole escape from protein catalytic sites on biologically relevant timescales. Furthermore, we find that pathways involving the [4Fe4S] cluster as the terminal hole acceptor in BSS are accessible on the millisecond timescale, suggesting a potential protective role of redox-active cofactors for preventing protein oxidative damage.

scholarly journals Selenium and vascular health

2011 ◽  
Vol 84 (2) ◽  
pp. 239-248 ◽  
Author(s):  
Alan A. Sneddon
Keyword(s):  
Oxidative Damage ◽  
Protective Role ◽  
The Body ◽  
Vascular Health ◽  
Vascular Cells ◽  
Optimal Health ◽  
Oxidative Challenge ◽  
Se Status

Selenium (Se) is an important dietary micronutrient required for sustaining optimal health. Se is incorporated into proteins, many of which are antioxidants that protect the body against oxidative damage. As oxidative damage may contribute to the development of chronic diseases including cardiovascular disease (CVD), Se has been proposed to provide a protective role against this disease. Studies in vitro and in animals continue to provide increasing insight into the role of Se in promoting vascular health and ameliorating CVD. Se within vascular cells limits the adhesion together of such cells, an important early step in the development of vascular disease. Organic forms of Se may also afford vascular cells greater protection against oxidative challenge compared to inorganic forms. Nevertheless, current studies in humans investigating the relationship between Se and CVD have so far proved equivocal; larger randomized trials with different Se exposures in populations spanning the broad physiological Se status are needed to determine the criteria whereby Se may influence CVD outcome within different populations. Further studies are also needed to explore the effects of different Se species and the role of different selenoprotein genotypes in modifying Se status and their resultant impact on cardiovascular function.

scholarly journals 4-Hydroxynonenal induces apoptosis in human osteoarthritic chondrocytes: the protective role of glutathione-S-transferase

2008 ◽  
Vol 10 (5) ◽  
pp. R107 ◽  
Author(s):  
France Vaillancourt ◽  
Hassan Fahmi ◽  
Qin Shi ◽  
Patrick Lavigne ◽  
Pierre Ranger ◽  
...  
Keyword(s):  
Protective Role ◽  
Glutathione S Transferase ◽  
Osteoarthritic Chondrocytes
Sign in / Sign up

Export Citation Format

Share Document