Melatonin Ameliorates Doxorubicin-induced Skin Necrosis in Rats
Malondialdehyde
DOI:
10.1097/sap.0b013e3181bb4b4e
Publication Date:
2010-06-26T08:52:18Z
AUTHORS (7)
ABSTRACT
Doxorubicin (DXR), a highly effective chemotherapeutic agent, causes serious injury when extravasated. The can sometimes result in skin necrosis and ulceration, requiring surgery. detrimental effect of DXR on the antioxidant system via free oxygen radicals is one mechanisms proposed its etiology. Thus, we used melatonin, potent antioxidant, compared effects with dimethylsulfoxide (DMSO), which treatment patients DXR-induced extravasation. Twenty-seven Wistar-albino rats were used. After intradermal injection DXR, DMSO was injected into extravasated area melatonin given intraperitoneally. On day 14 experiment, ulcers clearly formed samples taken punch biopsy. Ulcer sizes measured. Tissue analyzed for superoxide dismutase, glutathione peroxidase, malondialdehyde enzymes, histopathologically evaluated. Melatonin decreased MDA levels, ulcer size, histopathologic scores tissue. also size score. However, remarkably more than terms enzyme activity, oxidative stress, rats. Necrosis evident DXR-treated group some slides showed involving fascia. Histopathologic necrotic tissue groups. score significantly lower control group. Although control, there no statistically significant difference. both We believe that either alone or combination DMSO, may be treating In addition, play crucial role etiology injury, should considered further studies.
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