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Paraoxonase activity in the serum and hepatic mRNA levels decrease during the acute phase response

K R Feingold1, R A Memon, A H Moser

  • 1Department of Medicine, University of California San Francisco, Department of Veterans Affairs Medical Center 94121, USA.

Atherosclerosis
|August 26, 1998
PubMed
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Serum paraoxonase (PON) activity and PON1 mRNA levels decrease after endotoxin administration. This reduction, mediated by cytokines like TNF and IL-1, may link the acute phase response to increased atherosclerosis.

Area of Science:

  • Biochemistry
  • Immunology
  • Cardiovascular Science

Background:

  • Epidemiological studies suggest a link between the acute phase response and atherosclerosis.
  • Paraoxonase (PON) is an enzyme associated with HDL that protects LDL from oxidative stress.

Purpose of the Study:

  • To investigate the effect of endotoxin (LPS) administration on serum PON activity and hepatic PON1 mRNA levels in Syrian hamsters.
  • To determine the role of inflammatory cytokines (TNF and IL-1) in modulating PON activity and expression.

Main Methods:

  • Administration of endotoxin (LPS) to Syrian hamsters.
  • Measurement of serum PON activity.
  • Quantification of hepatic PON1 mRNA levels.
  • In vitro treatment of HepG2 cells with TNF and IL-1.

Related Experiment Videos

Main Results:

  • Serum PON activity significantly decreased within 24 hours after LPS administration.
  • Hepatic PON1 mRNA levels showed an 80% decrease as early as 4 hours post-LPS and remained suppressed for at least 48 hours.
  • Treatment with TNF and IL-1 decreased both serum PON activity and hepatic PON1 mRNA levels.
  • TNF and IL-1 directly reduced PON mRNA levels in HepG2 cells.

Conclusions:

  • Endotoxin administration leads to a significant decrease in serum PON activity and hepatic PON1 mRNA levels in Syrian hamsters.
  • Cytokines TNF and IL-1 mediate the reduction in PON activity and expression, suggesting a direct effect on liver cells.
  • The decrease in PON during the acute phase response may contribute to the association between inflammation and increased atherogenesis.