Original Article

Spinal Cord (2009) 47, 745–750; doi:10.1038/sc.2009.27; published online 2 June 2009

Deleterious versus neuroprotective effect of metabolic inhibition after traumatic spinal cord injury

S Torres1,2,3, H Salgado-Ceballos1,2, G Guizar-Sahagún1,2, J L Torres4, S Orozco-Suarez1, A Diaz-Ruiz5, M E Vázquez6, C Collado7 and C Ríos5

  1. 1Research Medical Unit in Neurological Diseases, CMN, S XXI, IMSS, Mexico city, Mexico
  2. 2Proyecto Camina AC, Mexico city, Mexico
  3. 3Department of Experimental Biology, Universidad Autónoma Metropolitana, Iztapalapa, Mexico city, Mexico
  4. 4Research Medical Unit in Oncological Diseases, CMN, S XXI, IMSS, Mexico city, Mexico
  5. 5Department of Neurochemestry, National Institute of Neurology and Neurosurgery, Mexico city, Mexico
  6. 6Research Medical Unit in Genetic Diseases, CMN, S XXI, IMSS, Mexico city, Mexico
  7. 7Manuelle Laboratories SA, Mexico city, Mexico

Correspondence: Dr H Salgado-Ceballos, Research Medical Unit in Neurological Diseases, CMN, S XXI, IMSS, Calle 25 No. 52, Col. Pro-Hogar, c.p. 02600, Azcapotzalco, Mexico city, Mexico. E-mail: hsalgadoc@cis.gob.mx

Received 30 September 2008; Accepted 24 February 2009; Published online 2 June 2009.

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Abstract

Study design:

 

This work is an experimental and prospective study in adult, female, Long–Evans rats.

Objectives:

 

The aim of this study was to probe the effect of metabolic inhibition after an acute traumatic spinal cord injury (TSCI) using a standardized contusion model (NYU impactor) to know whether the metabolic inhibition is a 'secondary mechanism of injury' or a mechanism of protection.

Setting:

 

All experimental procedures were carried out in the Mexico City.

Methods:

 

Animals were divided into five groups: one sham and four with TSCI, including no treatment, rotenone (inhibitor of mitochondrial complex I), sodium azide (inhibitor of mitochondrial complex IV) and pyrophosphate of thiamine or non-degradable cocarboxylase as a metabolic reactivator.

Results:

 

After TSCI, the metabolic inhibition with sodium azide treatment diminished the lipid peroxidation process (malondialdehyde levels by spectrophotometric procedures) and the damage to the spinal cord tissue (morphometric analysis), and increased the activity of creatine kinase and lactate dehydrogenase enzymes (P<0.05) (measured by spectrophotometric procedures 24 h after TSCI as well as after the functional recovery of the hind limb (evaluated weekly for 2 months by the BBB (Basso, Beattie and Bresnahan) scale)) when compared with the TSCI group without treatment.

Conclusion:

 

The results show that the partial and transitory inhibition of the aerobic metabolism after an acute TSCI could be a self-protection mechanism instead of being a 'secondary mechanism of injury'.

Keywords:

traumatic spinal cord injury, metabolic inhibition, rotenone, sodium azide, non-degradable cocarboxylase, lipid peroxidation

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