scholarly journals Serum Myeloperoxidase Activity, Total Antioxidant Capacity and Nitric Oxide Levels in Patients with Chronic Otitis Media

2013 ◽  
Vol 246 (7) ◽  
pp. 519-524 ◽  
Author(s):  
Mehmet Fatih Garça ◽  
Mehmet Aslan ◽  
Bakır Tuna ◽  
Ahmet Kozan ◽  
Hakan Cankaya
Author(s):  
Altug Kucukgul ◽  
Mehmet M. Isgor ◽  
Vesile Duzguner ◽  
Meryem N. Atabay ◽  
Azime Kucukgul

Background: Persistent oxidative stress can lead to chronic inflammation and mediate most chronic diseases including neurological disorders. Oleuropein has been shown to be a potent antioxidant molecule in olive oil leaf having antioxidative properties. Objective: The aim of this study was to investigate the protective effects of oleuropein against oxidative stress in human glioblastoma cells. Methods: Human glioblastoma cells (U87) were pretreated with oleuropein (OP) essential oil 10 µM. After 30 minutes, 100 µM H2O2 was added to the cells for three hours. Cell survival was quantified by colorimetric MTT assay. Glutathione level, total oxidant capacity, total antioxidant capacity and nitric oxide levels were determined by using specific spectrophotometric methods. The relative gene expression level of iNOS was performed by qRT-PCR method. Results: According to viability results, the effective concentration of H2O2 (100µM) significantly decreased cell viability and oleuropein pretreatment significantly prevented the cell losses. Oleuropein regenerated total antioxidant capacity and glutathione levels decreased by H2O2 exposure. In addition, nitric oxide and total oxidant capacity levels were also decreased after administration of oleuropein in treated cells. Conclusion: Oleuropein was found to have potent antioxidative properties in human glioblastoma cells. However, further studies and validations are needed in order to understand the exact neuroprotective mechanism of oleuropein.


Antioxidants ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 794 ◽  
Author(s):  
Celeste Santos-Rosendo ◽  
Fernando Bugatto ◽  
Alvaro González-Domínguez ◽  
Alfonso M. Lechuga-Sancho ◽  
Rosa Maria Mateos ◽  
...  

Pregnancy-related disorders, including preeclampsia and gestational diabetes, are characterized by the presence of an adverse intrauterine milieu that may ultimately result in oxidative and nitrosative stress. This scenario may trigger uncontrolled production of reactive oxygen species (ROS) such as superoxide anion (O●−) and reactive nitrogen species (RNS) such as nitric oxide (NO), along with an inactivation of antioxidant systems, which are associated with the occurrence of relevant changes in placental function through recognized redox post-translational modifications in key proteins. The general objective of this study was to assess the impact of a maternal obesogenic enviroment on the regulation of the placental nitroso-redox balance at the end of pregnancy. We measured oxidative damage markers—thiobarbituric acid-reacting substances (TBARS) and carbonyl groups (C=O) levels; nitrosative stress markers—inducible nitric oxide synthase, nitrosothiol groups, and nitrotyrosine residues levels; and the antioxidant biomarkers—catalase and superoxide dismutase (SOD) activity and expression, and total antioxidant capacity (TAC), in full-term placental villous from both pre-pregnancy normal weight and obese women, and with absence of metabolic complications throughout gestation. The results showed a decrease in C=O and TBARS levels in obese pregnancies. Although total SOD and catalase concentrations were shown to be increased, both activities were significantly downregulated in obese pregnancies, along with total antioxidant capacity. Inducible nitric oxide sintase levels were increased in the obese group compared to the lean group, accompanied by an increase in nitrotyrosine residues levels and lower levels of nitrosothiol groups in proteins such as ERK1/2. These findings reveal a reduction in oxidative damage, accompanied by a decline in antioxidant response, and an increase via NO-mediated nitrative stress in placental tissue from metabolically healthy pregnancies with obesity. All this plausibly points to a placental adaptation of the affected antioxidant response towards a NO-induced alternative pathway, through changes in the ROS/RNS balance, in order to reduce oxidative damage and preserve placental function in pregnancy.


2017 ◽  
Vol 4 (4) ◽  
pp. 1031
Author(s):  
Rohit Sheth ◽  
Tanmay Bhat ◽  
Suchetha Kumari N. ◽  
Harshini Devi Ullal

Background: The free radical theory of aging postulates that aging results from the accumulation of deleterious effects caused by free radicals, and the ability of an organism to cope with cellular damage induced by ROS plays an important role in determining organismal lifespan. GSH and SOD functions by donating the proton and in scavenging the superoxide radicals, thereby protecting the body against oxidative stress by scavenging the free radicals produced in the body. Glutathione peroxidase also have similar function, it reduce lipid hydroperoxides to their corresponding alcohols and free hydrogen peroxide to water.Methods: Hundred healthy adults from staff and student community under the age group of 20 to 60 years were recruited. Approximately 5ml blood sample was collected and used for the analysis of lipid profile, MDA and antioxidant status using standard protocol.Results: The lipid profile, MDA and antioxidant status were measured and compared with that of serum nitric oxide levels of 100 healthy individuals of the age 20-60 yrs. Men aged 20-29 years showed significantly higher NO levels compared to corresponding women. There is a significant reduction in total antioxidant capacity in elderly people. With the decrease in NO there is increase in MDA is observed.Conclusions: There is a significant reduction in total antioxidant capacity in elderly people. This reduction in antioxidant capacity implies a defect in antioxidant system, may be due to a reduction in individual antioxidant or may be caused by a non-equilibrium or poor cooperation between them.


2010 ◽  
Vol 30 (8) ◽  
pp. 897-903 ◽  
Author(s):  
Ahmet Gökçe ◽  
Suleyman Oktar ◽  
Ahmet Koc ◽  
Zafer Yonden

Thymoquinone is the major active component derived from Nigella sativa. Methotrexate is a folic acid antagonist widely used in clinic. Aim of this study was to investigate the possible protective role of thymoquinone on testicular toxicity of methotrexate. Experiments were performed on male C57BL/6 mice (6 weeks old, 20 ± 2 g). The animals were divided into four groups with six mice in each group. Equivalent volumes of saline were injected intraperitoneally (i.p.) in the control group. In the thymoquinone group, mice received thymoquinone i.p. with a dose of 10 mg/kg/day for 4 days. Mice in the methotrexate group received single dose of methotrexate i.p., with a dose of 20 mg/kg. Finally, in the methotrexate plus thymoquinone group, in the first and the following 3 days after methotrexate administration, thymoquinone was injected with a dose of 10 mg/kg/day, i.p. At the end of the experiment, the left testis was quickly removed and divided into two parts for histological examination and biochemical analysis. Methotrexate alone increased total antioxidant capacity and myeloperoxidase activity compared to the controls. Thymoquinone treatment decreased total antioxidant capacity and prevented the increase in the myeloperoxidase activity. Light microscopy showed in mice that receiving methotrexate resulted in interstitial space dilatation, edema, severe disruption of the seminiferous epithelium and reduced diameter of the seminiferous tubules. Administration of thymoquinone reversed histological changes of methotrexate significantly. We suggest that thymoquinone use may decrease the destructive effects of methotrexate on testicular tissue of patients using this agent.


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