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  • Open Access

Effects of neonatal hypoxia on mice behavior and oxidative stress parameters

  • 1,
  • 1,
  • 1 and
  • 1, 2
Annals of General Psychiatry20087(Suppl 1):S126

https://doi.org/10.1186/1744-859X-7-S1-S126

Published: 17 April 2008

Keywords

  • Catalase
  • Superoxide Dismutase
  • Locomotor Activity
  • Glutathione Peroxidase
  • Stress Parameter

Background

Approximately 2,9-9,0 of 1000 infants experience some degree of perinatal ischemic-anoxic or prolonged anoxic insult [1].

Materials and methods

Seven days old male Swiss mice were distributed on three groups: hypoxia (H), maternal separation (MS) and no handling (NH). H group underwent to 10% oxygen during 6 hours/day for 6 days and MS group was maintained in normoxia, but separated from their dams such as H group. When mice completed 3 months old, they were tested on locomotor activity boxes or in plus-maze. The parameters measured were erythrocyte catalase, superoxide dismutase and glutathione peroxidase (GPx) and cerebral catalase. Data were analyzed by one-way ANOVA test and Bonferroni post-hoc test, when appropriated.

Results

On the activity boxes, during the 5 first minutes, it was observed a significant decrease of vertical movements on H group, when compared to other groups. However, after 30 minutes, the groups didn't differ. Besides, H mice demonstrated a diverse emotionality on plus-maze, once the quantity of fecal boli and urine was significant different from group NH. Considering oxidative stress, only GPx values were increased on H group compared to MS group.

Conclusions

Neonatal hypoxia is capable of generating long-term alterations on mice behavior and on production and/or activation of some antioxidant enzymes.

Authors’ Affiliations

(1)
Department of Psychobiology, Federal University of Sγo Paulo, Sγo Paulo, Brazil
(2)
Department of Health Sciences, Federal University of Sγo Paulo, Sγo Paulo, Brazil

References

  1. Tuor UI, Del Bigio MR, Chumas PD: Brain damage due to cerebral hypoxia/ischemia in the neonate: pathology and pharmacological modification. Cerebrovasc Brain Metab Rev. 1996, 8 (2): 159-193.PubMedGoogle Scholar

Copyright

© Brandγo et al.; licensee BioMed Central Ltd. 2008

This article is published under license to BioMed Central Ltd.

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