Reported antioxidant, anti‐inflammatory and neuroprotective properties for one aqueous‐ethanolic extract from Thalassia testudinum which grows in the Caribbean Sea compelled us to explore about extract cytotoxic effects.
Methods
Cell viability was assayed on tumour (HepG2, PC12, Caco‐2 and 4T1) and non‐tumour (VERO, 3T3, CHO, MCDK and BHK2) cell lines. The extract effects upon primary cultures of rat and human hepatocytes and human lymphocytes were assayed.
Key findings
The extract exhibited cytotoxicity against cancer cells compared to normal cells, and the IC50 values were 102 μg/ml for HepG2, 135 μg/ml for PC12, 165 μg/ml for Caco‐2 and 129 μg/ml for 4T1 cells after 48 h, whereas IC50 could not be calculated for normal cells. Additional data from a high‐content screening multiparametric assay indicated that after 24‐h exposure, the extract (up to 100 μg/ml) induced death in HepG2 cells through oxidative stress‐associated mechanism, DNA damage and hypercalcaemia. Comet assay corroborated extract‐induced DNA damage.
Conclusions
Thalassia testudinum extract is more cytotoxic and produced more DNA damage on human hepatoma cells than to other non‐tumour cells. A possible mechanism is suggested for extract‐induced cytotoxicity based on oxidative stress, nuclear damage and hypercalcaemia in HepG2 cells. T. testudinum may be a source for antitumour agents.