Free radical scavengers can differentially modulate the genotoxicity of amsacrine in normal and cancer cells

Cytotoxic activity of acridin-3,6-diyl dithiourea hydrochlorides in human leukemia line HL-60 and resistant subline HL-60/ADR

“…Blasiak et al [13] showed that free radicals could be involved in the formation of DNA lesions induced by amsacrine and a freeradical based genotoxic potential of the drug can be modulated by some free-radical scavengers, e.g. vitamin E or thiols.…”

“…Amsacrine and its analogues have several mechanisms of action with topoisomerase II being a main target [12]. Blasiak et al [13] confirmed a possible modulation of amsacrine cytotoxicity by some free radical scavengers. Acridine analogues have also been evaluated for their strong DNA-binding activity [14] and cytotoxic potency toward sensitive and multidrugresistant tumor cell lines [15,16].…”

Impact of Single Nucleotide Polymorphisms of Base Excision Repair Genes on DNA Damage and Efficiency of DNA Repair in Recurrent Depression Disorder

“…DNA damage in PBMCs was estimated by the alkaline version (pH > 13) of the comet assay according to the procedure described by Singh et al with later modifications [22–24]. Since this technique recognizes only DNA strand breaks and alkali labile sites, two glycosylases—Nth or human 8-oxoguanine DNA glycosylase (endonuclease III and hOOG1, respectively; New England Biolabs, Ipswich, MA, USA)—were used to detect oxidative DNA damage according to the procedure described earlier [25].…”

DNA Interaction Studies and In Vitro Cytotoxicity of Newly Synthesized Steroidal Imidazolidinones

“…The planar imidazolidinone scaffold is being an important pharmacophore and potent fluorescent ligand intercalating between DNA base pairs and is often used in syntheses of antitumor DNA-targeting drugs [19]. Metal free imidazolidinone compounds are also able to inhibit topoisomerase I and II enzymes, render DNA damage, disrupt DNA repair and replication, and induce cell death without showing toxicity towards the normal cells [20,21]. It has also been found that the damage of DNA by these compounds is usually strengthened by the oxidative stress [21].…”

“…Metal free imidazolidinone compounds are also able to inhibit topoisomerase I and II enzymes, render DNA damage, disrupt DNA repair and replication, and induce cell death without showing toxicity towards the normal cells [20,21]. It has also been found that the damage of DNA by these compounds is usually strengthened by the oxidative stress [21]. The cytotoxicity of most imidazolidinone-based drugs is based on their ability to suppress topoisomerase activity [22].…”