Abstract
The study focuses on an in vivo GST- omega homologue (pCRT7/TPxII intB4) over-expression, purification and characterization. Experiments purport to characterize the antioxidant activity of the LeTPx1, the interacting glutathione S-transferases BI-GST/GPx, LeGST-T1, T2, T3, T4, T5 and the mammalian inhibitor of apoptosis Bcl-2. Upon specific expression, the proteins exerted, differential protective effects in yeast cells treated with lethal doses of the prooxidants hydrogen peroxide, t-butyl hydroperoxide, and cumene hydroperoxide. The antioxidant activity of LeTPx1 was highest against the cumene hydroperoxide. The overexpressing GST (omega) homologue TPxintB4 (Baier and Dietz, 1999) which share a considerable homology of the mammalian GST-omega1. In conclusion, the work shows that yeast parental strains are extremely sensitive to very low concentrations (0.2mM) of Cumenehydroperoxide. However, after applying the different antioxidants; it appears that the smallest concentrations t to be tolerated.
Highlights
Oxidative stress reproduces different range of systemic appearance of reactive oxygen species (ROS)
The implementing of the Two-Hybrid genomic screen afforded us with 26 proteins (Kampranis et al, 2000) that interact with LeTPx1.Our focus was on the over-expression and characterization of GST- omega homologue LeGSTO (Baier and Dietz, 1999) due to its significant biological and medical effects
LeGSTO1 was found to be capable of reducingan inter-subunit disulfide present in the oxidized form of LeTPx1
Summary
Oxidative stress reproduces different range of systemic appearance of reactive oxygen species (ROS). Disorders in the standard redox state of cells can lead to toxic properties through the creation of peroxides and free radicals that damage all mechanisms of the cell, including macromolecules synthesis, and DNA strand breaks. The destruction is mostly unintended and begins by reactive oxygen species (ROS) generated, e.g. O2− (superoxide radical), OH (hydroxyl radical) and H2O2 (hydrogen peroxide) (Kala, 2015) (ROS) act as cellular messengers in redox signaling. Production of reactive oxygen species is a predominantly damaging feature of oxidative stress. These active oxygen species consist of free radicals and peroxides. Some of the less reactive of these species (such as superoxide) can be converted by oxidoreduction reactions with transition metals or other redox cycling compounds (including quinones) into more aggressive radical species that can cause extensive cellular damage (Valko et al, 2005). In the severe ranks of oxidative stress that cause necrosis, the damage causes ATP reduction, inhibiting organized apoptotic death and causing the cell to just collapse (Lelli et al, 1998)
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