Melatonin protects against pressure ulcer-induced oxidative injury of the skin and remote organs in rats
Article first published online: 25 JAN 2006
Journal of Pineal Research
Volume 40, Issue 3, pages 280–287, April 2006
How to Cite
Şener, G., Sert, G., Özer Şehirli, A., Arbak, S., Gedik, N. and Ayanoğlu-Dülger, G. (2006), Melatonin protects against pressure ulcer-induced oxidative injury of the skin and remote organs in rats. Journal of Pineal Research, 40: 280–287. doi: 10.1111/j.1600-079X.2005.00313.x
- Issue published online: 22 FEB 2006
- Article first published online: 25 JAN 2006
- Received September 12, 2005; accepted November 30, 2005.
- decubitus ulcer;
- lipid peroxidation;
Abstract: Pressure ulcers (PU) cause morphological and functional alterations in the skin and visceral organs; the damage is believed to be due to ischemia/reperfusion (I/R) injury. In this study, we examined the role of oxidative damage in PU and the beneficial effect of treatment with the antioxidant melatonin. PU were induced by applying magnets over steel plates that were implanted under the skin of rats; this compressed the skin and caused ischemia. Within a 12-hr period, rats were subjected to five cycles of I/R (2 and 0.5 hr respectively), followed by an additional 12 hr of ischemia (to simulate the period at sleep at night). This protocol was repeated for 3 days. In treatment groups, twice a day during reperfusion periods, melatonin (5 mg per rat) was either applied locally as an ointment on skin, or administered i.p. (10 mg/kg). At the end of the experimental period, blood and tissue (skin, liver, kidney, lung, stomach, and ileum) samples were taken for determination of biochemical parameters and for histological evaluation. Local treatment with melatonin inhibited the increase in malondialdehyde levels; an index of lipid peroxidation, myeloperoxidase activity; an indicator of tissue neutrophil infiltration, and the decrease in glutathione; a key antioxidant, in the skin induced by PU, but was less efficient in preventing the damage in visceral organs. However, systemic treatment prevented the damage in the visceral organs. Significant increases in creatinine, blood urea nitrogen, alanine aminotransferase, aspartate aminotransferase, lactate dehydrogenase and collagen levels in animals with PU were prevented by melatonin treatment. The light microscopic examination exhibited significant degenerative changes in dermis and epidermis in the PU rats. Tissue injury was decreased especially in the locally treated group. Findings of the present study suggest that local and/or systemic melatonin treatment may prove beneficial in the treatment of PU.