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Severe toxicity and cyclooxygenase (COX)-2 mRNA increase by lithium in the neonatal mouse kidney

Wataru Yoshioka1, Toshiya Akagi, Noriko Nishimura

  • 1Center for Disease Biology and Integrative Medicine, Graduate School of Medicine, University of Tokyo, Bunkyo-ku, Tokyo, Japan.

The Journal of Toxicological Sciences
|October 3, 2009
PubMed

Insights

Neonatal mice exposed to lithium chloride experienced severe kidney damage, including cysts and hydronephrosis. This suggests cyclooxygenase-2 (COX-2) upregulation contributes to lithium

Area of Science:

  • Nephrology
  • Developmental Toxicology
  • Pharmacology

Background:

  • Neonatal kidney function is immature and vulnerable to chemical toxicants.
  • Cyclooxygenase (COX)-inducing chemicals are potential neonatal kidney toxicants.
  • Lithium chloride (LiCl) is investigated for its potential toxicity during the neonatal period.

Purpose of the Study:

  • To investigate the renal toxicity of LiCl in neonatal mice.
  • To explore the role of cyclooxygenase-2 (COX-2) in LiCl-induced kidney injury.

Main Methods:

  • Neonatal C57BL/J mice were injected with LiCl (2 mmol/kg) daily until 21 days of age.
  • Kidneys were examined at 7 and 21 days of age.
  • Measurements included COX-2 mRNA, aquaporin mRNA, urine osmolarity, and histological analysis.

Main Results:

  • LiCl treatment significantly increased COX-2 mRNA and decreased aquaporin mRNA on day 7.
  • Urine osmolarity was significantly lower in LiCl-treated neonates.
  • Histological examination revealed renal cysts and hydronephrosis; most LiCl-treated neonates died.

Conclusions:

  • Neonatal mouse kidneys are vulnerable to lithium exposure.
  • LiCl induces severe renal toxicity, including hydronephrosis.
  • COX-2 upregulation may be responsible for the observed renal toxicity.

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