Direct electric current treatment modifies mitochondrial function and lipid body content in the A549 cancer cell line

• Anodic flow treatment decreased A549 cell viability in a dose-dependent manner.
• Electrolytic treatment impaired tumor growth.
• Anodic flow treatment induced a two-fold increase in A549 caspase-3 activity.
• Anodic flow treatment triggered cellular and biochemical damage in tumor cells.

Electrochemical therapy (EChT) entails treatment of solid tumors with direct electric current (DC). This work evaluated the specific effects of anodic flow generated by DC on biochemical and metabolic features of the A549 human lung cancer cell line. Apoptosis was evaluated on the basis of caspase-3 activity and mitochondrial transmembrane potential dissipation. Cell morphology was analyzed using transmission electron microscopy, and lipid droplets were studied through morphometric analysis and X-ray qualitative elemental microanalysis. High-resolution respirometry was used to assess mitochondrial respiratory parameters. Results indicated A549 viability decreased in a dose-dependent manner with a prominent drop between 18 and 24 h after treatment (p < 0.001), together with a two-fold increase in caspase-3 activity. AF-treatment induced a significantly increase (p < 0.01) in the cell number with disrupted mitochondrial transmembrane potential. Furthermore, treated cells demonstrated important ultrastructural mitochondria damage and a three-fold increase in the cytoplasmic lipid bodies' number, quantified by morphometrical analyses. Conversely, 24 h after treatment, the cells presented a two-fold increase of residual oxygen consumption, accounting for 45.3% of basal oxygen consumption. These results show remarkable alterations promoted by anodic flow on human lung cancer cells which are possibly involved with the antitumoral effects of EChT.