Abstract

Marine organisms are a rich source of biologically active lipids with anti-inflammatory activities. These lipids may be enriched in visceral organs that are waste products from common seafood. Gas chromatography-mass spectrometry and fatty acid methyl ester (FAME) analyses were performed to compare the fatty acid compositions of lipid extracts from some common seafood organisms, including octopus (Octopus tetricus), squid (Sepioteuthis australis), Australian sardine (Sardinops sagax), salmon (Salmo salar) and school prawns (Penaeus plebejus). The lipid extracts were tested for anti-inflammatory activity by assessing their inhibition of nitric oxide (NO) and tumor necrosis factor alpha (TNFα) production in lipopolysaccharide (LPS)-stimulated RAW 264.7 mouse cells. The lipid extract from both the flesh and waste tissue all contained high amounts of polyunsaturated fatty acids (PUFAs) and significantly inhibited NO and TNFα production. Lipid extracts from the cephalopod mollusks S. australis and O. tetricus demonstrated the highest total PUFA content, the highest level of omega 3 (ω-3) PUFAs, and the highest anti-inflammatory activity. However, multivariate analysis indicates the complex mixture of saturated, monounsaturated, and polyunsaturated fatty acids may all influence the anti-inflammatory activity of marine lipid extracts. This study confirms that discarded parts of commonly consumed seafood species provide promising sources for the development of new potential anti-inflammatory nutraceuticals.

Highlights

  • Acute and chronic inflammation is the basis of many serious diseases including asthma, cardiovascular diseases, and rheumatoid arthritis [1]

  • Multivariate analysis indicates the complex mixture of saturated, monounsaturated, and polyunsaturated fatty acids may all influence the anti-inflammatory activity of marine lipid extracts

  • The lipid extracts from the cephalopod mollusks had the highest proportion of polyunsaturated fatty acids (PUFAs) comprising over 40% of the fatty acid composition (Figure 1B, Table 1)

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Summary

Introduction

Acute and chronic inflammation is the basis of many serious diseases including asthma, cardiovascular diseases, and rheumatoid arthritis [1]. The stimulation of macrophages during the inflammatory response gives rise to overproduction of several pro-inflammatory mediators, including nitric oxide (NO) via inducible nitric oxide synthase (iNOS) [2]. NO overproduction can lead to tissue damage through cytokine-mediated processes. This molecule can cause vasodilation, edema, and cytotoxicity [3,4]. Macrophage stimulation leads to the overproduction of many cytokines including TNFα and interleukins (IL). These pro-inflammatory cytokines have many roles, including the recruitment and activation of more macrophages, effects on the endothelial cells in the blood vessels, as well as playing a role in the perception of pain generated from inflammation [5].

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