The gallic acid and its derivatives have a diverse range of uses as antioxidants in food, cosmetics and pharmaceutical industries. Pharmaceutical studies performed with these compounds have found that they have many therapeutic potentialities including antitumoral, antiviral and antimicrobial properties. However, more interest has been devoted to their antioxidant activity due to the ability to scavenge and reduce reactive oxygen species (ROS) formation. Some works have demonstrated that gallic acid and its esters (methyl, propyl, octyl and lauryl-gallate induced apoptosis in different cell lines and lymphocyte proliferation inhibition. Chemical alterations at gallic acid molecule may modify the pharmacokinetic and pharmacodinamic proprieties, altering the solubility and the partition coefficient (P Log), consequently the biological properties. The new structures show different interactions with macromolecules and lipid membranes permeability. Therefore, in this study, we investigate the gallic acid and its esters cytotoxic effects towards B16F10 melanoma cells line.

B16F10 cells were incubated for 24h with gallic acid or with n-alquil-esters ( hexyl, heptyl, octyl, decyl, undecyl, dodecyl, tetradecyl and hexadecyl) in a range of 10 to 100mM. Cell viability was monitored through MTT assay, the apoptosis was analyzed by DNA fragmentation in 1,5% agarose gel eletrophoresis.

We observed that that all compounds induced cytotoxic effects on melanoma cells in a concentration-dependent manner. The higher cytotoxicity were observed with decyl and tetradecyl gallate witch reduced the number of viable cells in 70 ± 3% e 80 ± 1%, respectively, at 100mM,  when compared with the control (100% of viable cells). All compounds caused DNA fragmentation at 100mM after 24h of incubation.

The results suggest that n-alquil-esters of gallic acid caused apoptosis in B16F10 cells line and that decyl and tetradecyl gallate were more potent than the others, suggesting that there are relationship between the carbonic chain size  and cytotoxic effect.