Donmez Z, Yigit Ö, Bilici S, Dursun N, Gul M, Dastan S D, Uzun H
Department of Otorhinolaryngology, Istanbul Education and Research Hospital, Istanbul, Turkey.
Department of Pathology, Istanbul Education and Research Hospital, Istanbul, Turkey.
Clin Otolaryngol. 2016 Jun;41(3):211-21. doi: 10.1111/coa.12501. Epub 2016 Feb 4.
This study's aim was to investigate the effect of melatonin in terms of mitigating the effects of smoking on the laryngeal mucosa of rats exposed to environmental tobacco smoke.
Rats were divided into four groups: Melatonin + Smoking group exposed to smoke with melatonin; Smoking group exposed to smoke without melatonin; Saline group not exposed to smoke without melatonin; Melatonin group not exposed to smoke with melatonin. CuZn-superoxide dismutase (CuZn-SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities were evaluated in plasma and tissues. Tissues were also examined the changes of squamous hyperplasia, keratosis, parakeratosis and epithelial hyperplasia by light microscope and the ultrastructural changes by electron microscope.
Tissue SOD, CAT and GSH-Px activities were significantly higher in Saline and Melatonin groups than Melatonin + Smoking and Smoking groups. Plasma CuZn-SOD and CAT activities were significantly higher in Saline and Melatonin groups than Smoking group. Plasma GSH-Px showed no significant difference. The rate of epithelial hyperplasia was significantly higher in Smoking group than the other groups. The rate of parakeratosis was significantly higher in Smoking group than the other groups. The epithelial cells in Melatonin + Smoking group displayed, normal cell structure similar to those in Saline group under electron microscope.
The study shows that smoking induces substantial pathological changes in the laryngeal mucosa and melatonin may have some beneficial effects in partially reversing smoking-induced laryngeal injury by inducing the expression of antioxidants; biochemical and histological outcomes also support these findings due to preventing tissue damage in laryngeal mucosa exposed to smoke.
本研究旨在探讨褪黑素对减轻环境烟草烟雾暴露大鼠喉黏膜吸烟影响的作用。
将大鼠分为四组:褪黑素+吸烟组,暴露于烟雾且给予褪黑素;吸烟组,暴露于烟雾但不给予褪黑素;生理盐水组,不暴露于烟雾且不给予褪黑素;褪黑素组,不暴露于烟雾但给予褪黑素。评估血浆和组织中铜锌超氧化物歧化酶(CuZn-SOD)、过氧化氢酶(CAT)和谷胱甘肽过氧化物酶(GSH-Px)的活性。还通过光学显微镜检查组织鳞状上皮增生、角化、不全角化和上皮增生的变化,并通过电子显微镜检查超微结构变化。
生理盐水组和褪黑素组的组织SOD、CAT和GSH-Px活性显著高于褪黑素+吸烟组和吸烟组。生理盐水组和褪黑素组的血浆CuZn-SOD和CAT活性显著高于吸烟组。血浆GSH-Px无显著差异。吸烟组的上皮增生率显著高于其他组。吸烟组的不全角化率显著高于其他组。褪黑素+吸烟组的上皮细胞在电子显微镜下显示出与生理盐水组相似的正常细胞结构。
该研究表明,吸烟可导致喉黏膜发生大量病理变化,褪黑素可能通过诱导抗氧化剂表达对部分逆转吸烟引起的喉部损伤具有一些有益作用;生化和组织学结果也支持这些发现,因为其可防止暴露于烟雾的喉黏膜组织损伤。