Structural characteristics of native and chemically sulfated polysaccharides from seaweed and their antimelanoma effects.

Polysaccharides from seaweed have been shown to present a variety of antitumor effects, however the understanding of which structural patterns are responsible for these biological effects are still unclear. This review aimed to gather and critically evaluate published data of seaweed polysaccharide's chemical structure elucidation and their relation with antimelanoma effects. Data were collected at the electronic article databases Science Direct, NCBI/Pubmed and Google Scholar, selecting papers with polysaccharide structural information and biological effects on melanoma models. Most of the papers referred to sulfated polysaccharides as fucans and fucoidans, and to a lesser extent galactans, rhamnans, alginates, and neutral one's glucans. Fine chemical features as presence and position of sulfate groups, monosaccharide composition, linear or branched backbones, and glycosidic linkage type are crucial to antimelanoma effects, as well as molecular weight and macromolecular conformation.

Chemical structure of native and modified sulfated heterorhamnans from the green seaweed Gayralia brasiliensis and their cytotoxic effect on U87MG human glioma cells.

A water-soluble sulfated heterorhamnan (Gb1) was isolated from the green seaweed Gayralia brasiliensis and purified by ultrafiltration, yielding a homogeneous polysaccharide (Gb1r). Both fractions contained rhamnose, xylose, galacturonic and glucuronic acids, galactose, and glucose. Chemical and spectroscopic methods allowed the determination of Gb1 and Gb1r chemical structure. Their backbones were constituted by 3-, 2-, and 2,3-linked rhamnosyl units (1:0.49:0.13 and 1:0.58:0.17, respectively), which are unsulfated (13.5 and 14.6%), disulfated (16.6 and 17.8%) or monosulfated at C-2 (8 and 8.6%) and C-4 (24.5 and 23.4%). Gb1 was oversulfated giving rise to Gb1-OS, which presented ~2.5-fold higher content of disulfated rhamnosyl units than Gb1, as determined by methylation analyses and NMR spectroscopy. Gb1 and Gb1-OS potently reduced the viability of U87MG human glioblastoma cells. Gb1 caused cell cycle arrest in the G1 phase, increased annexin V-stained cells, and no DNA fragmentation, while Gb1-OS increased the percentage of cells in the S and G2 phases and the levels of fragmented DNA and cells double-stained with annexin V/propidium iodide, suggesting an apoptosis mechanism. The results suggest that the different effects of Gb1 and Gb1-OS were related to differences in the sulfate content and position of these groups along the polysaccharide chains.