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Rivista di Anestesia, Rianimazione, Terapia Antalgica e Terapia Intensiva

Official Journal of the Italian Society of Anesthesiology, Analgesia, Resuscitation and Intensive Care
Indexed/Abstracted in: Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 2,036

Periodicità: Mensile

ISSN 0375-9393

Online ISSN 1827-1596


Minerva Anestesiologica 2011 Giugno;77(6):571-8


Xenon exposure in the neonatal rat brain: effects on genes that regulate apoptosis

Cattano D. 1, Valleggi S. 2, Cavazzana A.O. 3, Patel C. B. 1, Ma D. 4, Giunta F. 5

1 Department of Anesthesiology, University of Texas Medical School at Houston, Houston, TX, USA;
2 Department of Physiology and Biochemistry, University of Pisa School of Medicine, Pisa, Italy;
3 Division of Surgical, Molecular and Ultrastructural Pathology, University of Pisa School of Medicine, Pisa, Italy;
4 Section of Anaesthetics, Pain and Intensive Care, Department of Surgery and Cancer, Imperial College London, Chelsea and Westminster Hospital, London, UK;
5 Postgraduate School of Anesthesiology and Critical Care, Department of Surgery, University of Pisa School of Medicine, Pisa, Italy

BACKGROUND: In the developing rodent brain, exposure to volatile anesthetics causes widespread neuronal apoptosis in several regions of the brain. Increasing evidence points to a possible neuroprotective role for the anesthetic gas xenon, following neuronal injury. To address this gap in understanding, we explored the transcriptional consequences of xenon in the brains of postnatal day 7 (P7) rats exposed to xenon compared to those of air-breathing animals, with particular emphasis on the mRNA transcript levels of Akt and c-Jun N-terminal kinase kinase 1 (JNKK1), which are important for cell survival and the activation of extrinsic neuroapoptotic pathways, respectively.
METHODS: P7 Sprague/Dawley rats were exposed to air (75% nitrogen, 25% oxygen) or xenon (75% xenon, 25% oxygen) for 120 min (N=6/group). Forebrains were harvested for reverse transcription polymerase chain reaction, which enabled quantification of Akt and JNKK1 mRNA transcripts. Suppression subtractive hybridization was used to explore the “genetic signature” of xenon exposure.
RESULTS: Compared to control air-breathing animals, xenon-breathing rats exhibited a 0.7-fold decrease in Akt mRNA expression (P<0.01) and a 1.6-fold increase in JNKK1 mRNA levels (P<0.05).
CONCLUSION: The concomitant decrease in the Akt mRNA expression level and increase in the JNKK1 mRNA transcript level provide evidence that xenon has a neuroapoptotic effect in the developing rodent forebrain. Given these results, further study into the paradoxical neuroprotective and neuroapoptotic effects of xenon is warranted.


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