ALPHA-TOCOPHEROL LIPOSOMES ALLEVIATE LPS-INDUCED HEPATOTOXICITIES

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Authors
  1. Suntres, Z.E.
  2. Shek, P.N.
Corporate Authors
Defence and Civil Inst of Environmental Medicine, Downsview ONT (CAN)
Abstract
Gram-negative bacteria, in part through lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF alpha), activate phagocytes to generate reactive oxygen species (ROS), which have been known to play a key role in the pathogenesis of liver injury. Accordingly, we hypothesized that the susceptibility of the liver to ROS should be reduced by augmenting its antioxidant status. Adult male Sprague-Dawley rats were pretreated with alpha-tocopherol liposomes (20 mg alpha-tocopherol/kg body weight, i.e.v), plain liposomes or saline, 24 h after liposomal treatment, rats were injected intravenously with LPS (1 mg/kg, Escherichia coli: 0111:B4) and killed 2 h later. Livers of saline-pretreated animals challenged with LPS were damaged as demonstrated by increases in plasma alanine aminotranferase (ALT) and aspartate aminotransferase (AST) activities. The hepatic injury appeared to be associated with oxidative stress-mediated mechanisms as evidenced by increase in lipid peroxidation and decreases in glutathione concentration in the liver, both indices of oxidative stress. Also, LPS injection resulted in increase in plasma TNF alpha and thromboxane B2 (TXB2) levels, as well as increase in hepatic myeloperoxidase (MPO) activity and chloramine concentration, suggestive of activation of the inflammatory response. TRUNCATED
Keywords
LipoPolySaccharide (LPS)
Report Number
DCIEM-96-RP-54 — Reprint
Date of publication
30 Apr 1996
Number of Pages
8
Reprinted from
Journal of Endotoxin Research, vol 3, no 6, 1996, p 505-512
DSTKIM No
97-01248
CANDIS No
501518
Format(s):
Hardcopy;Document Image stored on Optical Disk

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