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Hormonal and chemical regulation of paraoxonases in mice

Xingguo Cheng1, Curtis D Klaassen

  • 1Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, Kansas City, KS, USA.

The Journal of Pharmacology and Experimental Therapeutics
|June 2, 2012
PubMed

Insights

Female mice have higher liver paraoxonase-1 (PON1) expression due to male-pattern growth hormone (GH) inhibition. Constitutive androstane receptor (CAR) activation also decreases PON1 expression in mouse livers.

Area of Science:

  • Biochemistry
  • Genetics
  • Endocrinology

Background:

  • Paraoxonase (PON) enzymes are crucial in detoxification and lipid metabolism.
  • Gender-divergent expression of PON1 in liver and serum is observed in humans and rodents, but underlying mechanisms are unclear.
  • Regulation of PON1 by chemicals and sex hormones requires further investigation.

Purpose of the Study:

  • To elucidate the regulatory mechanisms behind gender-divergent and chemically altered PON1 expression in mouse livers.
  • To compare the expression patterns of PON1, PON2, and PON3 across different mouse tissues and developmental stages.
  • To investigate the role of growth hormone (GH) and nuclear receptors in modulating PON1 expression.

Main Methods:

  • Quantitative PCR (qPCR) and Western blotting were used to determine PON mRNA and protein levels in various mouse tissues and developmental stages.
  • Experiments involved administering male-pattern and female-pattern GH, sex hormones, and activators of aryl hydrocarbon receptor (AhR), pregnane X receptor (PXR), NF-E2-related factor (Nrf2), and constitutive androstane receptor (CAR).
  • Studies were conducted in wild-type mice, hypophysectomized mice, lit/lit mice, and CAR-null mice.

Main Results:

  • PON1 mRNA was most abundant in adult mouse livers, with higher levels in females than males. PON2 and PON3 were highly expressed in fetal liver and decreased postnatally.
  • Male-pattern GH administration significantly decreased PON1 expression in mouse livers, while sex hormones and female-pattern GH had no effect.
  • CAR activator reduced PON1 expression in wild-type mice but not in CAR-null mice, indicating CAR's inhibitory role.

Conclusions:

  • Female-predominant PON1 expression in adult mouse livers is attributed to the inhibitory influence of male-pattern GH secretion.
  • Constitutive androstane receptor (CAR) activation negatively regulates PON1 expression in mouse livers.
  • Developmental expression patterns of PON1, PON2, and PON3 differ significantly, with PON1 dominant in adult liver and PON2/PON3 in fetal liver.

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