Melatonin: a hepatoprotective agent against radioiodine toxicity in rats
BRATISLAVA MEDICAL JOURNAL-BRATISLAVSKE LEKARSKE LISTY, cilt.118, sa.2, ss.95-100, 2017 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 118 Sayı: 2
- Basım Tarihi: 2017
- Doi Numarası: 10.4149/bll_2017_020
- Dergi Adı: BRATISLAVA MEDICAL JOURNAL-BRATISLAVSKE LEKARSKE LISTY
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
- Sayfa Sayıları: ss.95-100
- Hatay Mustafa Kemal Üniversitesi Adresli: Evet
Özet
OBJECTIVES: The aim of the current study was to investigate the possible radioprotective effects of melatonin against hepatic radioiodine (RAI) toxicity. METHODS: Thirty-six rats were randomly divided into three groups: untreated control (Group 1); oral radioiodine (RAI, 111 MBq) administrated rats (Group 2), and melatonin group (oral RAI and daily intraperitoneal injection of 12 mg/kg melatonin-Group 3). In the third group, melatonin administration was started two days before and continued for five days after RAI administration. Twenty-four hours after the administration of the last dose of melatonin, liver samples were taken for biochemical and histopathological evaluation. RESULTS: Oxidative stress parameters demonstrated that melatonin treatment decreased the tissue malondialdehyde (MDA), advanced the oxidation protein products (AOPP) levels, and increased the total-SH (sulphydryl) levels when compared with RAI group. The differences were statistically significant between these groups for all parameters (p < 0.05). The histopathological damage in the melatonin-treated group was significantly less than the damage in RAI group (p < 0.05 for all pathological parameters). CONCLUSION: The results of this study demonstrated that melatonin reduced the harmful effects of RAI treatment on the liver. Anti-inflammatory and antioxidant activities are likely to be involved in the mechanism underlying the radio-protective effects of melatonin (Tab. 3, Fig. 1, Ref. 30). Text in PDF www.elis.sk.