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Review
. 2020 Jun 9;10(6):885.
doi: 10.3390/biom10060885.

Marine-Derived Surface Active Agents: Health-Promoting Properties and Blue Biotechnology-Based Applications

Ioannis Anestopoulos  1 , Despina-Evgenia Kiousi  1 , Ariel Klavaris  1 , Monica Maijo  2 , Annabel Serpico  2 , Alba Suarez  2 , Guiomar Sanchez  2 , Karina Salek  3 , Stylliani A Chasapi  4 , Aikaterini A Zompra  4 , Alex Galanis  1 , Georgios A Spyroulias  4 , Lourdes Gombau  2 , Stephen R Euston  3 , Aglaia Pappa  1 , Mihalis I Panayiotidis  5   6   7
Affiliations
Review

Marine-Derived Surface Active Agents: Health-Promoting Properties and Blue Biotechnology-Based Applications

Ioannis Anestopoulos et al. Biomolecules. .

Abstract

Surface active agents are characterized for their capacity to adsorb to fluid and solid-water interfaces. They can be classified as surfactants and emulsifiers based on their molecular weight (MW) and properties. Over the years, the chemical surfactant industry has been rapidly increasing to meet consumer demands. Consequently, such a boost has led to the search for more sustainable and biodegradable alternatives, as chemical surfactants are non-biodegradable, thus causing an adverse effect on the environment. To these ends, many microbial and/or marine-derived molecules have been shown to possess various biological properties that could allow manufacturers to make additional health-promoting claims for their products. Our aim, in this review article, is to provide up to date information of critical health-promoting properties of these molecules and their use in blue-based biotechnology (i.e., biotechnology using aquatic organisms) with a focus on food, cosmetic and pharmaceutical/biomedical applications.

Keywords: anti-aging; anti-cancer; anti-inflammatory; anti-microbial; anti-oxidant; anti-viral; biosurfactants; blue biotechnology; surface active agents.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Anti-inflammatory activity of marine-derived SAAs. Biosurfactants halt the production of pro-inflammatory mediators by interfering with pathways induced by the stimulation of Toll-like receptors, interleukin-1 receptor and Tumor Necrosis Factor-α receptor. These compounds directly inhibit key molecules of the IKK/NF-κΒ, p38 MAPK, MAPK/ERK and JNK signaling pathways or inactivate cyclooxynase-2 (COX-2) and 5-lipoxygenase (5-LOX) that catalyze the production of inflammatory molecules. TLR, Toll-like receptor; MD-2 (encoded by the LY96 gene): lymphocyte antigen 96; IL, interleukin; IL-1R, interleukin-1 receptor; MyD88, myeloid differentiation primary response 88; CIAP, calf intestinal alkaline phosphatase; RIP, ribosome-inactivating protein; TRIF, toll/interleukin-1 receptor-like protein (TIR)-domain-containing adaptor-inducing interferon-β; ΤRAM, TRIF-related adaptor molecule; TRAF, tumor necrosis factor receptor-associated factor; TAB1/2, tumor growth factor-β (TGF-β)-activated kinase 1; TAK, TGF-β activated kinase 1; IKK, IκΒ kinase; MKK, mitogen activated protein (MAP) kinase; COX-2, cyclooxygenase-2; 5-LOX, 5-lipoxygenase; iNOS, inducible nitrogen oxide synthase; NF-κΒ, nuclear factor κΒ; ΕRK, extracellular signal activated kinase; JNK, c-Jun N-terminal kinase; AP-1, activator protein-1; IRAK, IL-1 receptor associated kinase.
Figure 2
Figure 2
Anti-cancer activity of marine-derived SAAs through induction of both intrinsic and extrinsic apoptotic pathways. Biosurfactants exhibit considerable anti-cancer activity by inhibition of the MAPK/ERK and Akt/PI3K signaling pathways, as well as through suppression of nuclear antigens, MKI67 and PCNA. Their anti-cancer capacity is also mediated through reduced expression of MMPs-2 and -9 known to be associated with tumor metastasis. RTK, Receptor tyrosine kinase; PI3K, Phosphatidylinositol-3-Kinase; MAPK, Mitogen-activated protein kinase; ERK, Extracellular signal–regulated kinase; MEK, MAPK/ERK kinase; PIP2, Phosphatidylinositol 4,5-bisphosphate; PIP3, Phosphatidylinositol (3,4,5)-trisphosphate; NF-kB, Nuclear factor kappa-light-chain-enhancer of activated B cells; FOXO3a, Forkhead box O3a; GSK3β, Glycogen synthase kinase 3 beta; MKI67, Marker of Proliferation Ki-67; PCNA, Proliferating Cell Nuclear Antigen; PARP, Poly (ADP-ribose) Polymerase; Bid, BH3-interacting domain death agonist; tBid, truncated Bid; Bcl-2, B-cell lymphoma 2; BCL-XL, B-cell lymphoma-extra-large; BAX, BCL2 associated X; BAK, BCL2-antagonist/killer; ROS, Reactive oxygen species; Smac/DIABLO, Second mitochondria-derived activator of caspase/direct inhibitor of apoptosis-binding protein with low pI; IAPs, Inhibitors of apoptosis protein; Apaf-1, Apoptotic protease activating factor 1; MMP-2, Matrix metalloproteinase-2; MMP-9, Matrix metalloproteinase-9; ECM, Extracellular matrix.
Figure 3
Figure 3
Anti-cancer activity of marine-derived SAAs through regulation of cell cycle progression. Surfactin and fucoidan exhibit anti-cancer activity by blocking cell cycle progression through up-regulation of inhibitor(s) levels of CDKs. In addition, fucoidan induce G1 phase cell cycle arrest, through inhibition of RB phosphorylation. pRB, phosphorylated retinoblastoma; CDKs 4,2,1, Cyclin-dependent kinases 4,2,1; E2F, E2 promoter binding Factor.
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