Abstract
The antioxidant activities of Tabebuia impetiginosa methanolic extract (TIME) were examined with its serial solvent extracts using hexane, chloroform and ethyl acetate against hydrogen peroxide (H2O2)-induced oxidative stress in NIH3T3 cells. The three serial extracts were selected for the study of regeneration on antioxidant enzyme activities because butanol and water extracts significantly affected cell survival. Treatment of hydrogen peroxide on the cells showed a dramatic repression on superoxide dismutase (SOD) and cytosolic NADPH+-dependent isocitrate dehydrogenase (IDPc) activities with the remaining activities of 56.1 and 37.5%, respectively. The three extracts significantly regenerated SOD activity with the range of 103 to 178% when compared to the control, and IDPc activity with the range of 34.4 to 42.2%. The three extracts also regenerated catalase and glucose-6-phosphate dehydrogenase activities with the range of 91.6 to 139% in comparison to the control. Hydrogen peroxide did not change intracellular glutathione content. The three serial extracts of TIME enhanced intracellular glutathione concentration, protected proteins from the oxidative attack by H2O2 and also decreased malonaldehyde formation in the cells. Taken together, the non-polar extracts of TIME protect NIH3T3 cells from the H2O2-induced oxidative stress. Key words: Tabebuia impetiginosa, NIH3T3, antioxidant activity, hydrogen peroxide (H2O2), lipid peroxidation.
Highlights
For the living organisms, an imbalance of redox state between the production of reactive oxygen species (ROS) and removal of the ROS is referred to as oxidative stress and a biological system induces its ability to detoxify the reactive intermediates and to prevent or repair the resulting damage to cells
The purpose of this study was to assess the antioxidant effects of Tabebuia impetiginosa methanolic extract (TIME) as the regeneration of non-enzymatic and enzymatic defense systems on oxidative stress induced by hydrogen peroxide (H2O2) using NIH3T3 cells
To evaluate the cytotoxicity against cell damage induced by H2O2, cells were exposed to H2O2 and treated with the solvent serial fractions of TIME, whereas control cells were treated with H2O2 in the presence and the cells were incubated of vehicle only
Summary
An imbalance of redox state between the production of reactive oxygen species (ROS) and removal of the ROS is referred to as oxidative stress and a biological system induces its ability to detoxify the reactive intermediates and to prevent or repair the resulting damage to cells. Hydrogen peroxide (H2O2, a wellknown oxidant) is generated in vivo by the dismutation of superoxide radicals via superoxide dismutase enzymes. Most biological systems have shown their peculiar adaptation to recover from a variety of oxidative stress with the development of an effective and complicated network for defense mechanisms, to efficiently handle the harmful oxidative environments (Ames et al, 1993; Fridovich, 1978; Lundberg and Weitzberg, 2010). These defense mechanisms include non-enzymatic and enzymatic defenses. The non-enzymatic systems include reduced glutathione (GSH), ascorbic acid, α-tocopherol, uric acid, and small peptide thioredoxin, while enzymatic defenses include superoxide dismutases (SOD), catalases (CAT), and peroxidases (Chance et al, 1979; McCord and Fridovich, 1969)
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