AIM: To study the protective role of melatonin (MT) in peroxynitrite-induced injury in cultured aortic smooth muscular cells (ASMC). METHODS: Peroxynitrite was synthesized chemically with a quenched flow reaction. Cells were exposed to peroxynitrite 500 μmol/L for 1 h in the absence or presence of various concentrations of MT 100, 300, and 500 μmol/L. Nitrotyrosine (NT), a specific “footprint” of peroxynitrite formation, was detected by immunohistochemical technique. The DNA damage was assayed by TUNEL technique. The levels of MDA in the medium and cell viability were measured. RESULTS: Incubation of ASMC with peroxynitrite 500 μmol/L for 1 h elicited the increase in the extent of immunostaining for NT, the rate of the TUNEL-positive cell, the content of MDA in the medium, and the number of dead cell. Pretreatment of ASMC with MT 100-500 μmol/L decreased these peroxynitrite-induced changes in a concentration-dependent manner. CONCLUSION: MT attenuated the injury induced by peroxynitrite in ASMC. AIM: To study the protective role of melatonin (MT) in peroxynitrite-induced injury in cultured aortic smooth muscular cells (ASMC). METHODS: Peroxynitrite was synthesized with a quenched flow reaction. Cells were exposed to peroxynitrite 500 μmol / L for 1 h in the absence or presence of various concentrations of MT 100, 300, and 500 μmol / L. Nitrotyrosine (NT), a specific “footprint” of peroxynitrite formation, was detected by immunohistochemical technique. The DNA damage was assayed by TUNEL technique. The levels of MDA in the medium and cell viability were measured. RESULTS: Incubation of ASMC with peroxynitrite 500 μmol / L for 1 h elicited the increase in the extent of immunostaining for NT, the rate of the TUNEL-positive cell, the content of MDA in the medium, and the number of dead cells. Pretreatment of ASMC with MT 100-500 μmol / L decreased these peroxynitrite-induced changes in a concentration-dependent manner. CONCLUSION: MT attenuated the suspension induce d by peroxynitrite in ASMC.