Protective Effect of Amifostine against Etoposide-Induced Genotoxicity Evaluated By the Comet Assays

Nasrin Ghassemi-Barghi,Mohammad Shokrzadeh

doi:10.15226/2374-6866/5/3/00184

Abstract

Protective Effect of Amifostine against Etoposide-Induced Genotoxicity Evaluated By the Comet Assays

Highlights

Etoposide is an anticancer drug used alone or in combination with other drugs in chemotherapy of testicular cancer, lung cancer, lymphoma, leukemia, neuroblastoma and ovarian cancer [1,2,3,4,5]
Results of the visual scoring and percentage of total DNA damage induced by etoposide and prevented by amifostine were shown in Table 1.We observed that etoposide treatment at 1μM induced a significant (p < 0.001) increase in DNA damage as compared to the control group
We have demonstrated that amifostine protected Hepg2 cells against etoposide -induced DNA damage and oxidative injury

Summary

Introduction

Etoposide is an anticancer drug used alone or in combination with other drugs in chemotherapy of testicular cancer, lung cancer, lymphoma, leukemia, neuroblastoma and ovarian cancer [1,2,3,4,5]. Former studies reported an acute myeloid leukemia as a secondary cancer subsequent treatment by etoposide. Etoposide is involved in secondary malignancies because of its genotoxic potential in normal tissues[9, 10]. As a potent topoisomerase inhibitor, etoposide can cause DNA damage by generating a “lesion” that includes DNA strand breaks and protein covalently bound to DNA.[13].Several in vitro and in vivo reports have shown that etoposide induce apoptosis and senescence in different cell lines. Etoposide has shown diverse genotoxic effects including mutation induction and several complaints in DNA synthesis in numerous animal and cell line studies [10, 17]. The genotoxicity of etoposide have been evidenced in chromosome aberration tests, micronucleus assays and comet assay in various studies [10, 18, 19]. Second malignancies detected in patients earlier treated with topoisomerase II interactive agents propose these may be a significant clinical outcome of their ability to induce mutation[20]

Objectives

Methods

Results

Discussion

Conclusion