role of caspases and reactive oxygen species in rose bengal-induced toxicity in melanoma cells

نویسندگان

s. h. mousavi assistant professor of pharmacology, pharmacological research centre of medicinal plants, school of medicine, mums, mashhad, iran

p. hersey professor of immunology and oncology, newcastle mater hospital, newcastle, nsw, australia.

چکیده

objective we have previously shown that rose bengal (rb) alone, not as a photosensitiser, could induce apoptotic- and non-apoptotic cell death in different melanoma cell lines. to clarify rb-induced toxicity mechanisms, role of caspases and reactive oxygen specious (ros) were studied in melanoma cells. material and methods human melanoma cell lines, me 4405 and sk-mel-28 were cultured in dmem medium. cell viability was quantitated by mtt assay. apoptotic cells were determined using pi staining of dna fragmentation by flow cytometry (sub-g1 peak). role of caspase were studied using the pan-caspase inhibitor, z-vad-fmk. ros was measured using dcf-da by flow cytometry analysis. results this study showed that whilez-vad-fmk completely inhibited apoptosis of melanoma inducedby tumor necrosis factor (tnf)-related apoptosis-inducing ligand(trail), it only partiallyblocked rb-induced apoptosis in me4405 and sk-mel-28 melanoma cell lines. rb also increased ros production in melanoma cells but pretreatment with antioxidant -glutamylcysteinylglycine (gsh) could not decrease rb-induced toxicity. conclusion both caspase-dependent and -independent pathways were inducedby rb in melanoma cells. rb-induced generation of ros does not playa significant role in rb-induced toxicity and it is independent of ros production in melanoma cells.

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عنوان ژورنال:
iranian journal of basic medical sciences

جلد ۱۰، شماره ۲، صفحات ۱۱۸-۱۲۳

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