Turkish Journal of Medical Sciences




Recent evidance supports the concept that Epirubicin-HCI and Lymphokine-activated killer cells (LAK) cytotoxicity may be mediated by free radical and oxyradical generation. We tested this hypothesis further by exposing Hep G2 cells to Epirubicin-HCI and LAK cells and subsequently monitored cell viability as a measure of cytotoxicity. The cytotoxicity of LAK alone and LAK together with low dose epirubicin-HCI (IC50 1/10) which is measured using the MTT cytotoxicity test on viability of Hep G2 cells and sensitization of target cells to effector cells was investigated. The cytotoxicity of LAK (IC50 value of 5LAK/Hep G2 in 24 hours) and LAK+epirubicin-HCI (IC50 value of 2.5LAK+epirubicin-HCI/Hep G2 cell in 24 hours) appeared to involve a free radical species production type of mechanism since free radicals scavenger enzymes activity, Mn-SOD, Cu,Zn-SOD, Se-dependent GPx and catalase, were increased (p


Hepatoma, epirubicin-HCI, cytotoxicity, enzymes

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