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Neurol Res. 2012 Jan;34(1):59-67. doi: 10.1179/1743132811Y.0000000060.

Ozone oxidative post-conditioning reduces oxidative protein damage in patients with disc hernia.

Author information

1
Department of Pharmacology/Toxicology from Institute of Pharmacy and Food Sciences, University of Havana, Cuba. olga@infomed.sld.cu

Abstract

INTRODUCTION/OBJECTIVES:

Although inflammation in disc hernia (DH) has been recognized and it is a well-known process mediated by loss of the cellular redox balance, only a few studies about the impact of chronic oxidative stress on this neurological disorder have been made. Ozone therapy has been widely used with clinical efficacy in DH. This work aimed at characterizing the systemic redox status of patients with low back pain and neck pain as well as studying if ozone oxidative post-conditioning modified the pathological oxidative stress and protected against oxidative protein damage and if there is any relationship between oxidative changes and pain in both DH.

METHODS:

Redox status of 33 patients with diagnosis of DH by computerized axial tomography, nuclear magnetic resonance, and clinical evaluations was studied. Ozone was administered by paravertebral way. After ozone treatment, plasmatic levels of antioxidant/pro-oxidant markers, pain, and life quality disability parameters were evaluated.

RESULTS:

One hundred percent of patients showed a severe oxidative stress. Major changes in superoxide dismutase activity, total hydroperoxides, advanced oxidation protein products, fructolysine content, and malondialdehyde were observed. After ozone oxidative post-conditioning, there was a re-establishment of patients' cellular redox balance as well as a decrease in pain in both DH. A relationship between indicators of oxidative protein damage and pain was demonstrated.

CONCLUSIONS:

Ozone therapy protected against oxidation of proteins and reduced the pain. Relationship between markers of oxidative protein damage, disability parameters, and pain suggests the role of oxidative stress in the pathological processes involved in DH.

PMID:
22196863
DOI:
10.1179/1743132811Y.0000000060
[Indexed for MEDLINE]

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