Abstract
SummaryIt has been shown previously that molecules built on benzanilide and thiobenzanilide scaffolds possess differential biological properties including selective anticancer activity. In our previous study, we examined the cytotoxic activity and mechanism of action of the thiobenzanilide derivative N,N′-(1,2-phenylene)bis3,4,5–trifluorobenzothioamide (63 T) as a potential chemotherapeutic compound in an experimental model employing A549 lung adenocarcinoma cells and CCD39Lu non-tumorigenic lung fibroblasts. Since the results suggested oxidative stress as a co-existing mechanism of the cytotoxic effect exerted by 63 T on tested cells, studies involving the analysis of reactive oxygen species (ROS) generation and markers of oxidative stress in cells incubated with 63 T were carried out. It may be concluded that the selective activity of 63 T against cancer cells shown in our experiments is caused, at least in part, by the response of the tested cells to 63 T mediated oxidative stress in both tested cell lines.
Highlights
Oxidative stress is a fundamental concept in redox biology and medicine
All experiments were performed using two cell lines: A549 and CCD39Lu. Both cell lines were obtained from the European Collection of Authenticated Cells Cultures (ECACC, Salisbury, UK) and cultured in Dulbecco’s Modified Eagle’s Medium (DMEM) without phenol red supplemented with 10% FBS, 1% penicillin/streptomycin and 1% L-glutamine at 37 °C Gibco Invitrogen Corp. (Grand Island, NY, USA), in a humidified atmosphere containing 5% CO2
The increase of reactive oxygen species (ROS) in CCD39Lu cells was observed for doses of 0.25 μM, 0.5 μM and 1 μM by 61%, 90%, 50% respectively, compared with the control, the ROS generation was lower compared to A549 cells
Summary
Oxidative stress is a fundamental concept in redox biology and medicine. It is defined as Ban imbalance between oxidants and antioxidants in favor of the oxidants, leading to a disruption of redox signaling and control and/or molecular damage^ [1]. Numerous studies shed light on the important role of the overproduction of reactive oxygen species (ROS) in the development of different types of cancer, as this increases DNA mutations and damage, increasing the tendency for alterations in the genome and cancer cell growth and preventing cell death [6, 7]. It is well known that a moderate increase of ROS production may stimulate cell proliferation while an excessively high increase corresponds to several abnormalities and decreases viability [8]. An antioxidant treatment is considered as chemoprevention which may potentially protect from oxidative injuries, it should be emphasized that, depending on several circumstances, the use of antioxidants may have an adverse effect by promoting cancer cell survival [9, 10]
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