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  • Title: Staphylococcus aureus infection induced redox signaling and DNA fragmentation in T-lymphocytes: possible ameliorative role of nanoconjugated vancomycin.
    Author: Chakraborty SP, Das S, Chattopadhyay S, Tripathy S, Dash SK, Pramanik P, Roy S.
    Journal: Toxicol Mech Methods; 2012 Apr; 22(3):193-204. PubMed ID: 22074192.
    Abstract:
    Staphylococcus aureus is most frequently isolated pathogen causing bloodstream infections, skin and soft tissue infections and pneumonia. Vancomycin sensitive and resistant S. aureus infection causes oxidative stress in neutrophils and lymphocytes. Lymphocyte is an important immune cell. The immune cells use reactive oxygen species (ROS) for carrying out their normal functions while an excess amount of ROS can attack cellular components that lead to cell damage. The aim of the present study was to test the protective role of nanoconjugated vancomycin against Vancomycin Sensitive S. aureus (VSSA) and Vancomycin Resistant S. aureus (VRSA) infection induced oxidative stress in T-lymphocytes. VSSA and VRSA infection were developed in Swiss mice by intraperitoneal injection of 5 × 10(6) CFU/ml bacterial solutions. Nanoconjugated vancomycin was treated to VSSA and VRSA infected mice at a dose of 100 mg/kg bw/day and 500 mg/kg bw/day, respectively for successive 10 days. Vancomycin was treated to VSSA and VRSA infected mice at similar dose, respectively, for 10 days. The result of this study reveals that in vivo VSSA and VRSA infection significantly increases the level of nitrite generation, lipid peroxidation, protein oxidation, oxidized glutathione level, DNA fragmentation, and decreases the level of reduced glutathione, antioxidant enzyme status, glutathione dependent enzymes as compared to control group; which were increased or decreased significantly near to normal in T-lymphocytes of nanoconjugated vancomycin treated group. These finding suggests the potential use and beneficial protective role of nanoconjugated vancomycin against VSSA and VRSA infection induced oxidative stress in T-lymphocytes.
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