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Hepatic DNA fragmentation

Further study demonstrated that THS significantly inhibited hepatic DNA fragmentation, the emergence of apoptotic bodies and chromatin condensation in D-GalN/LPS-induced liver injury in mice. The extent of the inhibitory effect of THS on hepatocyte apoptosis at 5 hr paralleled that on serum ALT elevation at 8 hr [87]. As mentioned above, in this model, a large number of hepatocytes undergoing apoptotic cell death can... [Pg.467]

Fig. 6. The role of endogenous tumor necrosis factor TNF) in D-galactosamine (GalN)-induced liver damage. All mice were injected with 2.1 g/kg GalN. Serum transaminases ALT) and hepatic DNA fragmentation were determined after 24 h. Animals pretreated with neutralizing anti-TNF antibodies or mice lacking TNF receptor-1 tnf-rl°) were protected... Fig. 6. The role of endogenous tumor necrosis factor TNF) in D-galactosamine (GalN)-induced liver damage. All mice were injected with 2.1 g/kg GalN. Serum transaminases ALT) and hepatic DNA fragmentation were determined after 24 h. Animals pretreated with neutralizing anti-TNF antibodies or mice lacking TNF receptor-1 tnf-rl°) were protected...
No changes in hepatic DNA fragmentation were observed in rats fed diets containing 0 to 2.5% of an Indian frankincense extract containing 30% 3-O-acetyl-ll-keto-P-boswellic acid daily for 90 days (Lalithakumari et al. 2006). [Pg.145]

Ray SD, et al. (1992) Ca-activated DNA fragmentation and dimethylnitrosamine-induced hepatic necrosis Effects of Ca -endonuclease and poly(ADP-ribose) polymerase inhibitors in mice. Journal of Pharmacology and Experimental Therapeutics 263(1) 387-394. [Pg.1842]

Su F, Schneider RJ (1997) Hepatitis B virus HBx protein sensitizes cells to apoptotic killing by tumor necrosis factor alpha. Proc Natl Acad Sci USA 94 8744-8749 Sun DY, Jiang S, Zheng L, Ojcius DM, Young JD (1994) Separate metabolic pathways leading to DNA fragmentation and apoptotic chromatin condensation. J Exp Med 179 559-568... [Pg.153]

Berven et al. described the toxic effects induced by OA after intravenous injection in rats (100-200 g). The toxin (50-500 4g/kg) had little effect on intestinal function, but caused liver damages. At doses of 0.2 pg/kg or more, rats became inactive, cyanotic, and died within few hours. Autopsy and histological examination revealed a pronounced congestion of blood in the liver and a dissolution of hepatic bile canalicular actin sheaths, but neither the microtubular nor the keratin network of hepatocytes was affected by the toxin. Similarly, administration of OA did not induce apoptotic DNA fragmentation in hepatocytes. [Pg.242]

Shara, M., S.E. Ohia, T. Yasmin, et al. 2003. Dose- and time-dependent effects of a novel (-)-hydroxycitric acid extract on body weight, hepatic and testicular lipid peroxidation, DNA fragmentation and histopathological data over a period of 90 days. Mol. Cell. Biochem. 254(l-2) 339-346. [Pg.393]

Oxidative stress induced by chronic administration of naphthalene (llOmg/kg rat x day p.o. in corn oil up to 120 days) resulting in tissue damaging effects as maximum increases in hepatic and brain lipid peroxidation and DNA fragmentation was reported by Bagchi et al. (1998). [Pg.184]

Tan, W. G. lyrrell, D. L. J. Dovichi, N. J. Detection of duck hepatitis B virus DNA fragments using on-column intercalating dye labeling with capillary electrophoresis-laser-induced fluorescence. J. Chromatogr., A 1999, 853, 309-319. [Pg.381]


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See also in sourсe #XX -- [ Pg.466 , Pg.467 , Pg.468 , Pg.469 , Pg.472 ]

See also in sourсe #XX -- [ Pg.25 , Pg.466 , Pg.467 , Pg.468 , Pg.469 , Pg.472 ]




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