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Beneficial properties of melatonin in an experimental model of pancreatic cancer
Author(s) -
RuizRabelo Juan F.,
Vázquez Reyes,
Perea María D.,
Cruz Adolfo,
González Raul,
Romero Ana,
MuñozVillanueva María C.,
Túnez Isaac,
Montilla Pedro,
Muntané Jordi,
Padillo Francisco Javier
Publication year - 2007
Publication title -
journal of pineal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 131
eISSN - 1600-079X
pISSN - 0742-3098
DOI - 10.1111/j.1600-079x.2007.00472.x
Subject(s) - melatonin , oxidative stress , medicine , endocrinology , superoxide dismutase , pancreatic cancer , glutathione peroxidase , pancreas , antioxidant , glutathione , catalase , cancer , chemistry , biochemistry , enzyme
Pancreatic cancer is a major health problem because of the aggressiveness of the disease and the lack of effective systemic therapies. Melatonin has antioxidant activity and prevents experimental genotoxicity. However, the effect of melatonin in pancreatic cancer has not been tested. Pancreatic carcinogenesis was induced by N ‐nitrosobis (2‐oxopropyl)amine (BOP) in Syrian hamsters. Melatonin was administered during the BOP‐induction phase (12 wk) and/or following the postinduction phase (12 wk). Different parameters of oxidative stress including lipid peroxides (LPO) and antioxidants (superoxide dismutase, catalase, reduced glutathione and glutathione peroxidase) were determined in pancreatic tissue. Also, the presence of atypical hyperplasia (AH), well and moderately differentiated adenomacarcinoma (ADC‐WD and ADC‐MD, respectively) were studied. The administration of BOP induced an intense oxidative stress and ADC induction in the pancreas. The administration of melatonin during the induction or postinduction phase reduced LPO and improved the antioxidant status, as well as drastically reducing the presence of ADC but some AH remained. In conclusion, treatment with melatonin reduced oxidative damage and cancer nodules induced by BOP in the pancreas.