Spinal levels of nonprotein thiols are related to nociception in mice

Oxidative stress markers are thought to be related to nociception. Because thiolic compounds are important antioxidants, we investigated the relationship between thiols, endogenous or exogenous, and nociception. Systemic or spinal, but not peripheral, administration of the exogenous thiolic compound...

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Bibliographic Details
Published in:	The journal of pain Vol. 11; no. 6; p. 545
Main Authors:	Rossato, Mateus Fortes, Velloso, Nádia Alesso, de Oliveira Ferreira, Ana Paula, de Mello, Carlos Fernando, Ferreira, Juliano
Format:	Journal Article
Language:	English
Published:	United States 01-06-2010
Subjects:	Acetylcysteine - administration & dosage Acetylcysteine - pharmacology Acute Disease Analgesics - administration & dosage Analgesics - pharmacology Animals Antimetabolites - pharmacology Arthritis, Experimental - complications Arthritis, Experimental - drug therapy Arthritis, Experimental - metabolism Behavior, Animal - drug effects Buthionine Sulfoximine - pharmacology Capsaicin Disease Models, Animal Female Foot Injuries - complications Foot Injuries - drug therapy Foot Injuries - metabolism Lipid Peroxidation - drug effects Lipid Peroxidation - physiology Lumbar Vertebrae Male Mice Oxidative Stress - drug effects Oxidative Stress - physiology Pain - drug therapy Pain - etiology Pain - metabolism Spinal Cord - drug effects Spinal Cord - metabolism Sulfhydryl Compounds - administration & dosage Sulfhydryl Compounds - metabolism Sulfhydryl Compounds - pharmacology
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Summary:	Oxidative stress markers are thought to be related to nociception. Because thiolic compounds are important antioxidants, we investigated the relationship between thiols, endogenous or exogenous, and nociception. Systemic or spinal, but not peripheral, administration of the exogenous thiolic compound N-acetyl-L-cysteine (NAC) reduced nociception induced by intraplantar capsaicin injection. Moreover, we detected an increase in lipid peroxidation and 3-nitrotyrosine and a decrease in nonprotein thiolic levels in the lumbar spinal cord of capsaicin-injected animals. All these effects were prevented by NAC treatment (i.p. and i.t.). Our findings confirm a role for the spinal cord in NAC actions because systemic NAC administration also reduced the nociception trigged by intrathecal injection of capsaicin. Moreover, adjuvant-induced arthritis, but not paw incision, also -decreases nonprotein thiol levels in the spinal cord. Similarly, NAC produced antinociception in adjuvant-treated animals, but not in paw-incised animals. Finally, we investigated the role of endogenous thiol compounds in the nociceptive process administrating buthionine-suphoxamine (BSO), an inhibitor of glutathione-synthesis. Intrathecal BSO treatment decreased nonprotein thiol levels in the spinal cord, as well as induced mechanical allodynia and chemical and thermal hyperalgesia. In conclusion, our results indicate a critical role for nonprotein thiols in nociception at the level of the spinal cord. The results presented here indicate that the loss of nonprotein thiols in the spinal cord is involved in pain development. Therefore, the administration of thiolic compounds or other strategies allow thiol levels to be maintained and could be a beneficial action in the therapy of painful conditions.
ISSN:	1528-8447
DOI:	10.1016/j.jpain.2009.09.016