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Iron oxide nanoparticles and magnetic field exposure promote functional recovery by attenuating free radical-induced damage in rats with spinal cord transection

Authors Pal A, Singh, Nag T, Chattopadhyay, Mathur R, Jain S

Received 20 February 2013

Accepted for publication 27 March 2013

Published 21 June 2013 Volume 2013:8(1) Pages 2259—2272


Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2

Ajay Pal,1 Anand Singh,2 Tapas C Nag,3 Parthaprasad Chattopadhyay,2 Rashmi Mathur,1 Suman Jain1

1Department of Physiology, 2Department of Biochemistry, 3Department of Anatomy, All India Institute of Medical Sciences, New Delhi, India

Background: Iron oxide nanoparticles (IONPs) can attenuate oxidative stress in a neutral pH environment in vitro. In combination with an external electromagnetic field, they can also facilitate axon regeneration. The present study demonstrates the in vivo potential of IONPs to recover functional deficits in rats with complete spinal cord injury.
Methods: The spinal cord was completely transected at the T11 vertebra in male albino Wistar rats. Iron oxide nanoparticle solution (25 µg/mL) embedded in 3% agarose gel was implanted at the site of transection, which was subsequently exposed to an electromagnetic field (50 Hz, 17.96 µT for two hours daily for five weeks).
Results: Locomotor and sensorimotor assessment as well as histological analysis demonstrated significant functional recovery and a reduction in lesion volume in rats with IONP implantation and exposure to an electromagnetic field. No collagenous scar was observed and IONPs were localized intracellularly in the immediate vicinity of the lesion. Further, in vitro experiments to explore the cytotoxic effects of IONPs showed no effect on cell survival. However, a significant decrease in H2O2-mediated oxidative stress was evident in the medium containing IONPs, indicating their free radical scavenging properties.
Conclusion: These novel findings indicate a therapeutic role for IONPs in spinal cord injury and other neurodegenerative disorders mediated by reactive oxygen species.

Keywords: secondary damage, oxidative stress, electromagnetic field, cytotoxicity, neurodegeneration, pain

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