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J Neurol Surg A Cent Eur Neurosurg 2013; 74(03): 136-145
DOI: 10.1055/s-0033-1337607
Original Article
Georg Thieme Verlag KG Stuttgart · New York

Tobacco-Induced Neuronal Degeneration via Cotinine in Rats Subjected to Experimental Spinal Cord Injury

Ali Dalgic
1   Neurosurgery Clinic, Ankara Numune Research and Training Hospital, Yenimahalle, Ankara, Turkey
,
Onder Okay
1   Neurosurgery Clinic, Ankara Numune Research and Training Hospital, Yenimahalle, Ankara, Turkey
,
Fatma Helvacioglu
2   Department of Histology and Embryology, School of Medicine, Gazi University, Ankara, Turkey
,
Ergun Daglioglu
1   Neurosurgery Clinic, Ankara Numune Research and Training Hospital, Yenimahalle, Ankara, Turkey
,
Rifat Akdag
1   Neurosurgery Clinic, Ankara Numune Research and Training Hospital, Yenimahalle, Ankara, Turkey
,
Gulnur Take
2   Department of Histology and Embryology, School of Medicine, Gazi University, Ankara, Turkey
,
Deniz Belen
1   Neurosurgery Clinic, Ankara Numune Research and Training Hospital, Yenimahalle, Ankara, Turkey
› Author Affiliations
Further Information

Publication History

06 March 2011

23 December 2011

Publication Date:
19 March 2013 (online)

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Abstract

Objectives Cigarette smoke contains over 4000 chemicals including well-characterized toxicants and carcinogens, among which is cotinine. Cotinine is the principal metabolite of nicotine that has adverse affects on the microcirculation via vasoconstriction, hypoxia and the wound-healing cascade. Its impact on spinal cord injury (SCI) has not been investigated yet. The aim of the present study is to investigate the cotinine effect on SCI.

Methods 48 male Wistar rats were divided into six groups as follows: sham-control, sham-trauma, vehicle-control, vehicle-trauma, cotinine-control, and cotinine-trauma. Initially, a defined concentration of cotinine blood level was maintained by daily intraperitoneal injection of cotinine for 14 days in the cotinine groups. The concentration was similar to the cotinine dose in the blood level of heavy smokers. Only ethyl alcohol was injected in the vehicle groups during the same period. Then, SCI was performed by a Tator clip. The cotinine groups were compared with rats subjected to vehicle and sham groups by immunohistochemical biomarkers such as glial fibrillary acidic protein (GFAP) and 2,3-cyclic nucleotide 3-phosphodiesterase (CNP) expressions. Electron microscopic examination was also performed.

Results GFAP-positive cells were noted to be localized around degenerated astrocytes. Marked vacuolization with perivascular and perineural edema was seen in the cotinin consumption groups. These findings showed the inhibition of regeneration after SCI. Similarly, vacuolization within myelin layers was noted in the cotinine groups, which was detected through reduced CNP expression.

Conclusion Cotinine, a main metabolite of nicotine, has harmful effects on SCI via GFAP and CNP expression. The findings of the present study support the hypothesis that tobacco causes neuronal degeneration via cotinine.

Keywords

tobacco - cotinine - neuronal degeneration - spinal cord injury
 

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