Search

The cytotoxicity of three species of New Zealand (NZ) surf clam extracts was investigated in three hormonal cancer cell lines. Four extracts from each clam species were used: water, ethanol, petroleum ether (pe), and ethyl acetate (ea). The last three of these extracts significantly induced apoptosis via caspase cascades and cell cycle arrest. This was observed, for example, in the percentages of early apoptotic cells in Storm shell extracts with PC-3, MCF-7, and SiHa, with 30, 31, and 35%, respectively, at 400 μg∙ml-1. Cells incubated for 72 h led to the induction of arrest in the S- and G2-M phases. Previous analysis showed that pe and ea extracts from NZ clams were rich in lipids, and current indications based on fractional efficacy, pointed to a lipid soluble bioactive compound. This study provided a basis for further development of NZ clam extracts for treatment, or as a supplement, for positively affecting prostate, breast, and cervical cancers. • The anticancer activity of New Zealand surf clam species was studied. • New Zealand surf clam extracts induced apoptosis in cancer cell lines in vitro. • Differences in chemical composition led to anticancer activity of extracts. • Cytotoxicity increased with an increase in concentration and time. [ABSTRACT FROM AUTHOR]

Fucoidan, the complex fucose-containing sulphated polysaccharide varies considerably in structure, composition, and bioactivity, depending on the source, species, seasonality, and extraction method. In this study, we examined five fucoidans extracted from the same seaweed species Undaria pinnatifida but from different geological locations, and compared them to the laboratory-grade fucoidan from Sigma (S). The five products differed in molecular composition. The amount of over 2 kDa low molecular weight fraction (LMWF) of the New Zealand crude fucoidan (S1) was larger than that of S, and this fraction was unique, compared to the other four fucoidans. The difference of molecular compositions between S and S1 explained our previous observation that S1 exhibited different anticancer profile in some cancer cell lines, compared with S. Since we observed this unique LMWF, we compared the cytotoxic effects of a LMWF and a high molecular weight fucoidan (HMWF) in two breast cancer cell lines-MCF-7 and MDA-MB-231. Results indicated that the molecular weight is a critical factor in determining the anti-cancer potential of fucoidan, from the New Zealand U. pinnatifida , as the LMWF exhibited a dose-dependent inhibition on the proliferation of breast cancer cells, significantly better than the HMWF, in both cell lines. A time-dependent inhibition was only observed in the MCF-7. Induction of caspase-dependent apoptosis was observed in the MDA-MB-231 cells, through the intrinsic apoptosis pathway alone, or with the extrinsic pathway. LMWF stimulated a dose-dependent NOS activation in the MDA-MB-231 cells. In conclusion, the fucoidan extracted from the New Zealand U. pinnatifida contains a unique LMWF, which could effectively inhibit the growth of breast cancer cell lines. Therefore, the LMWF from New Zealand U. pinnatifida could be used as a supplement cancer treatment.