*4.6. Anticancer Properties*

For several decades, macroalgae have been promoted for their potential role in preventing cancer occurrence, tumor progression, and even health recovery after radio- or chemotherapy treatments [78,136]. Iodine may also exert an anticancer e ffect, due to the ability to cause apoptosis in cancer cells. The same property can be attributed to the omega-3 fatty acids such as stearidonic acid and hexadecatetraenoic acid found in edible marine algae such as *Undaria* and *Ulva* up to 40% of total fatty acids [140].

Alginate, laminaran, fucoidan, and many other seaweed polysaccharides were proven to have antitumor activities. A high amount of polysaccharide (~65% of polysaccharide in total dry weight) can be found in the many seaweeds such as *Ulva, Ascophyllum, Porphyra*, and *Palmaria* [141]. Alginate is able to clean up the intestinal tract, therefore improving immunity and intestinal tract health levels, reducing the risk of cancer. Laminaran and fucoidan are able to induce apoptosis in order to prevent cancer, but some unidentified seaweed polysaccharides can also exhibit direct or indirect antitumor e ffects. *Sargassum latifolium* inhibited cytochrome P450 1A and glutathione S-transferases and reduced 1301 cell viability, inducing apoptosis [142]. *Ulva fasciata* extract inhibits the growth of tumor cells in human colon cancer by 50% at a concentration of 200 μg/mL [143]. *Gracilariopsis lemaneiformis* was shown to have antitumor activity by inducing apoptosis in several cancer cell lines (e.g., human lung cancer cell line A549, the gastric cancer cell line MKN28, and the mouse melanoma cell line B16) attributed to neutral polysaccharide with a linear structure of repeated disaccharide agarobiose units [144]. Furthermore, the extracts of *Hydroclathrus clathratus* and its purified polysaccharide fractions were able to suppress the ascitic Sarcoma 180 tumor growth and prolonged the life span of the tumor-bearing mice with 30–40%, while presenting low toxicity to the normal cells [145].

Fucoidans extracted from *Dictyota ciliolata*, *Padina sanctae-crucis*, and *Sargassum fluitans* brown algae were reported to possess a high antioxidant activity being able to protect HepG2 cells from oxidative stress. Moreover, at a concentration of 2mg/mL, none of the fucoidan extracts had cytotoxic effects [146]. The isolated fucoidan from *Sargassum polycystum* exhibited potent antioxidant, anticancer, and antiproliferative properties against human breast cancer cell line MCF 7 at 150 g/mL and an IC50 of 50 g/mL [147]. Fucoidans from *Fucus evanescens* at a concentration of 800 μg/mL were reported to have anticancer properties by inhibiting the proliferation of melanoma SK-MEL-28 cell [148]. These findings underline once more that algae fucoidans are worth considering for the development of functional food, supplements, or drugs that can be used in the prevention of oxidative stress induced diseases.

The administration of extracts of the red alga *Eucheuma cottonii* to rats significantly improved the oxidative state of cells, and contributed to the tumor suppression response against MB-MDA-431 cell lines [149].

Meroditerpenoids are reported to be present mostly in brown algae. Metabolites such as fallahydroquinone, fallaquinone, fallachromenoic acid, sargaquinone, sargaquinoic acid, sargahydroquinoic acid, and sargachromenol were identified from the *Sargassum fallax* brown algae and reported to possess lower to moderate antitumor activity against a P388 Murine Leukaemia cell line [150].

## *4.7. Anti-Inflammatory Property*

Inflammation is one of the most complex medical problems. It can be initiated by several factors, namely environmental pollution, chemical intoxication, and bacterial infection, which lead to injury or death of cells. Approximately 20% of all human cancers are caused due to chronic inflammation [151]. Several studies on the anti-inflammatory e ffect of di fferent species of algae are listed in Table 2 below.


**Table 2.** The anti-inflammatory e ffect of di fferent species of algae.


#### **Table 2.** *Cont.*
