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The aim of the present study was to develop a new experimental pain model by adapting the chronic constriction injury (CCI) model of the sciatic nerve to the exclusively sensory saphenous nerve in rats. Animals were divided into naïve, sham, and two experimental groups, in which two or four 4-0 chromic gut ligatures were loosely ligated around the saphenous nerve. Then, behavioral signs of neuropathic pain were observed for 8 weeks. In rats with four ligatures, prominent mechanical allodynia and thermal hyperalgesia developed; these behavioral signs were not prominent in rats with two ligatures. Pharmacological analysis was made in rats with four loose ligations; morphine and WIN 55,212-2, a cannabinoid agonist, reversed all of the modalities tested, whereas gabapentin only suppressed mechanical allodynia and amitriptyline only reduced mechanical hyperalgesia. Our data establish a rat model of saphenous CCI with significant allodynia and hyperalgesia, which is sensitive to a number of analgesic compounds.

Objective: DNA damage that can be caused by workplace exposure to antineoplastic drugs in health workers has been shown in many scientific studies. It is aimed to evaluate whether the risk of genotoxicity in health workers decreases after the regulations and measures taken by national and international health authorities in our work. Methods: For this purpose, DNA damage was assessed by using alkaline comet technique in lymphocytes isolated from blood samples of health workers (n=29) who were involved in preparing and / or administering antineoplastic agent at Trakya University Health Research and Application Center and compared with the control group (n=30). Also, those who prepare and/or administer antineoplastic agents; (n=16) and manual (n=13) preparations. Results: As a result of the evaluation, there was no statistically significant difference between health personnel and control group in preparing and / or administering antineoplastic agent (p>0,05, Mann-Whitney U) and there was no difference in the genotoxic risk between preparation forms. Furthermore, when the exposed control group was assessed for DNA damage as smokers and nonsmokers, there was no statistically significant difference in terms of DNA damage (p>0.05). Conclusion: At the center where our samples were taken, the resulting measures resulted in the control of the risk of genotoxicity due to occupational exposure to antineoplastic agents.