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- W825526064 abstract "Studies presented in this dissertation determined biochemical mechanisms underlying the modulation of chemical-induced liver injury by retinol and GdClsThe first objective was to determine the role of inflammatory cells in the retinol potentiation of CCU-induced liver injury. Plasma alanine aminotranferase activities and histological analysis of liver sections both illustrated significant potentiation of CCI4 hepatotoxicity by a single dose of retinol. The mechanism for this potentiation involves priming of Kupffer cells (KC) (i.e. by enhancing their response to toxic stimuli) as established by chemical inhibitors of KC, isolated KC, and immunohistochemical analysis of liver sections. Additional studies estimated the effect of retinol on non-inflammatory processes (i.e. cytochrome P450 (P450) activity). While total P450 content was not increased, the activity and concentration of CYP 2E1 were both significantly elevated following treatment with a single dose of retinol. These findings suggest that a single pretreatment with retinol potentiates CCI4 hepatotoxicity by multiple mechanisms that involve increased biotransformation and inflammatory cell activities. Based on the findings with retinol, another immunomodulating agent. GdCb. might also alter the activity of hepatic biotransforming enzymes. Having established that GdCb inhibits the activity of KC, the purpose of these studies was to determine the effect of GdCb on the content and activity of hepatic P450. GdCb treatment reduced total hepatic microsomal P450 as well as aniline hydroxylase activity by 30% in male and 20% in female rats. Hepatocytes isolated fiom rats pretreated with GdCls were less susceptible" @default.
- W825526064 created "2016-06-24" @default.
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- W825526064 date "1998-01-01" @default.
- W825526064 modified "2023-09-27" @default.
- W825526064 title "Alterations in chemically-induced liver injury by immunomodulators" @default.
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