BACKGROUND: The purpose of this study was to evaluate in vitro cytotoxicity and antifibrotic effects of mitomycin C on normal and scarred human vocal fold fibroblasts. METHODS: Fibroblasts were subjected to mitomycin C treatment at 0.2, 0.5, or 1 mg/mL, or serum control. Cytotoxicity, immunocytochemistry, and Western blot for collagen I/III were performed at days 0, 1, 3, and 5. RESULTS: Significant decreases in live cells were measured for mitomycin C-treated cells on days 3 and 5 for all doses. Extracellular staining of collagen I/III was observed in mitomycin C-treated cells across all doses and times. Extracellular staining suggests apoptosis with necrosis, compromising the integrity of cell membranes and release of cytosolic proteins into the extracellular environment. Western blot indicates inhibition of collagen at all doses except 0.2 mg/mL at day 1. CONCLUSION: A total of 0.2 mg/mL mitomycin C may provide initial and transient stimulation of collagen for necessary repair to damaged tissue without the long-term risk of fibrosis.
BACKGROUND: The purpose of this study was to evaluate in vitro cytotoxicity and antifibrotic effects of mitomycin C on normal and scarred human vocal fold fibroblasts. METHODS: Fibroblasts were subjected to mitomycin C treatment at 0.2, 0.5, or 1 mg/mL, or serum control. Cytotoxicity, immunocytochemistry, and Western blot for collagen I/III were performed at days 0, 1, 3, and 5. RESULTS: Significant decreases in live cells were measured for mitomycin C-treated cells on days 3 and 5 for all doses. Extracellular staining of collagen I/III was observed in mitomycin C-treated cells across all doses and times. Extracellular staining suggests apoptosis with necrosis, compromising the integrity of cell membranes and release of cytosolic proteins into the extracellular environment. Western blot indicates inhibition of collagen at all doses except 0.2 mg/mL at day 1. CONCLUSION: A total of 0.2 mg/mL mitomycin C may provide initial and transient stimulation of collagen for necessary repair to damaged tissue without the long-term risk of fibrosis.
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