4.4 Article

Assessment of the cytotoxic potential of an aqueous-ethanolic extract from Thalassia testudinum angiosperm marine grown in the Caribbean Sea

Journal

JOURNAL OF PHARMACY AND PHARMACOLOGY
Volume 70, Issue 11, Pages 1553-1560

Publisher

WILEY
DOI: 10.1111/jphp.13001

Keywords

cytotoxicity; DNA damage; oxidative stress; Thalassia testudinum

Funding

  1. Visiting Research Program [400768/2014-3] Funding Source: Medline
  2. Environmental Agency, Ministry of Science, Technology and Environmental of Cuba (CITMA) Funding Source: Medline
  3. IIS La Fe Hospital, Valencia, Spain Funding Source: Medline
  4. VLIR TEAM/Own Initiatives-Programme [ZEIN2016PR420] Funding Source: Medline

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ObjectivesReported 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. MethodsCell 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 findingsThe extract exhibited cytotoxicityagainst cancer cells compared to normal cells, and the IC50 values were 102g/ml for HepG2, 135g/ml for PC12, 165g/ml for Caco-2 and 129g/ml for 4T1 cells after 48h, 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 100g/ml) induced death in HepG2 cells through oxidative stress-associated mechanism, DNA damage and hypercalcaemia. Comet assay corroborated extract-induced DNA damage. ConclusionsThalassia 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.

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