The potential inflammatory role of arginase and iNOS in children with chronic adenotonsillar hypertrophy.
OBJECTIVE
Nitric oxide (NO) induced tissue damage has been implicated in the pathogenesis of several diseases. Although recurrent/chronic tonsillitis and hypertrophy are still the most frequent surgical procedures carried out on children in order to cure these pathologies, etiopathogenetic mechanisms underlying these entities are still unknown. We aimed to investigate the potential inflammatory role of NO regulatory enzymes, arginase and inducible nitric oxide synthase (iNOS), in children with adenotonsillar hypertrophy.


METHODS
The study consisted of 22 children with chronic adenotonsillar hypertrophy and 30 control subjects with similar age and sex. All the patients and/or their parents had complaints of snoring, mouth breathing and pausing of breathe during sleep at least 6 months. All patients underwent an adenotonsillectomy operation under general anesthesia with curettage and cold dissection methods. Venous blood samples were taken pre-operatively and 4 weeks post-operatively. iNOS activity was based on the diazotization of sulfanilic acid by nitric oxide at acid pH and subsequent coupling to N-(1-naphthtyl)-ethylenediamine. Arginase activity was measured by the spectrophotometric method.


RESULTS
The mean pre-operative and post-operative arginase activities in patient group were 4283.7 +/- 1823.7 and 2754.5 +/- 889.3 IU/L, respectively. In the control group, mean arginase activity was 2254.7 +/- 903 IU/L. When pre-, post-operative and control arginase values were compared with each other, the mean activity in pre-operative activity was significantly different from the post-operative and control values (p < 0.001). In the patient group, the mean levels of pre- and post-operative iNOS were 2.84 +/- 1.16 and 1.99 +/- 0.78 IU/ml, respectively. The difference was statistically significant (p = 0.007). Similarly, post-operative and control values were not significantly different (p > 0.05).


CONCLUSIONS
The results of the present study supports that L-arginine:NO pathway may be key the participant in the pathogenesis of chronic adenotonsillar disease; arginase and iNOS activities are altered in children with adenotonsillar hypertrophy and this alteration improves after tonsillectomy.
Unal
Murat
M
Department of Otorhinolaryngology, School of Medicine, Mersin University, Mersin, Turkey. munal@mersin.edu
Cimen
M Y Burak
MY
Doğruer
Zeynep Nil
ZN
Cevik
Tugay
T
D000233:Adenoidectomy; D000234:Adenoids / Q000201:enzymology* / Q000473:pathology* / Q000601:surgery; D001119:Arginase / Q000378:metabolism*; D002648:Child; D002908:Chronic Disease; D005260:Female; D006801:Humans; D006984:Hypertrophy / Q000201:enzymology / Q000473:pathology / Q000601:surgery; D008297:Male; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D011182:Postoperative Care; D011300:Preoperative Care; D014068:Tonsillectomy; D014069:Tonsillitis / Q000201:enzymology* / Q000473:pathology* / Q000601:surgery
D019001:Nitric Oxide Synthase; D001119:Arginase