Please use this identifier to cite or link to this item: http://nopr.niscpr.res.in/handle/123456789/23387
Title: Oxidative and non-oxidative activation of murine peritoneal macro phages by histone H1
Authors: Vani, G
Deepa, C N
Devi, C S Shyamala
Keywords: Cytolysis;Glutathione;Histone H1;L929 cells;Lysosomal enzymes;Macrophages
Issue Date: Mar-2004
Publisher: NISCAIR-CSIR, India
Abstract: The present study aimed at assessing the role of histone H1 in activating macrophages. Hi stone H1, injected intraperitoneally at a dose of 1mg/kg body weight as multiple regime ns weekly, significantly increased the number of peritoneal macrophages post 21 days of injection. The oxidative and non-oxidative activation of peritoneal macrophages by histone H1 was assessed. For the assessment of oxidative activation the levels of superoxide radical and nitric oxide radical were assessed. The oxidative activation was evident from release of significantly high levels of superoxide and nitric oxide radicals liberated by macrophages of animals treated with hi stone H1 (P < 0.001) than in untreated animals. In addition, the higher activities of superoxide dismutase indicated protective effect of histone H1, to keep away the macrophages from noxious effects of superoxide. The catalase activity was decreased significantly in macrophages of histone H1 treated animals. The levels of reduced glutathione were significantly (P < 0.001) lowered in treated animals, whereas the levels of lipid peroxides generated were non-significant. The non-oxidative activation was assessed from the activities of lysosomal enzymes released and also from cytolysis of NO-insensitive L929 cells. The activities of lysosomal enzymes-acid phosphatase and β-glucuronidase released were significantly high in treated animals than in untreated animals (P < 0.001). Histone H1 stimulated the cytolysis of macrophages in L929 cells than in untreated animals. These results suggest that histone H1 stimulates macrophages by oxidative and non-oxidative mechanisms, which favor its future therapeutic prospects.
Page(s): 265-270
ISSN: 0975-1009 (Online); 0019-5189 (Print)
Appears in Collections:IJEB Vol.42(03) [March 2004]

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