No abstract

No abstract

In recent years, new approaches have been developed to limit the oxidation of oil-based food products by inhibiting peroxidation at the interfacial region. This review article describes and discusses these particular approaches. In bulk oils, modifying the polarity of antioxidants by chemical methods (e.g., esterifying antioxidants with fatty alcohol or fatty acids) and combining antioxidants with surfactants with low hydrophilic–lipophilic balance value (e.g., lecithin and polyglycerol polyricinoleate) can be effective strategies for inhibiting peroxidation. Compared to monolayer emulsions, a thick interfacial layer in multilayer emulsions and Pickering emulsions can act as a physical barrier. Meanwhile, high viscosity of the water phase in emulsion gels tends to hinder the diffusion of pro-oxidants into the interfacial region. Furthermore, applying surface-active substances with antioxidant properties (such as proteins, peptides, polysaccharides, and complexes of protein-polysaccharide, protein-polyphenol, protein-saponin, and protein-polysaccharide-polyphenol) that adsorb at the interfacial area is another novel method for enhancing oil-in-water emulsion oxidative stability. Furthermore, localizing antioxidants at the interfacial region through lipophilization of hydrophilic antioxidants, conjugating antioxidants with surfactants, or entrapping antioxidants into Pickering particles can be considered new strategies for reducing the emulsion peroxidation.

Background: Nephrotoxicity is a major side effect of aminoglycoside antibiotics, caused by oxidative damage and inflammation. Fucoidan, a group of sulfated polysaccharides derived from different species of brown algae, are well recognized for their antioxidant and anti-inflammatory activities. Objectives: In the present study, we aimed to investigate, for the first time, the efficacy of fucoidan extracted from Sargassum angustifolium C. Agardh 1820 against gentamicin-induced nephrotoxicity in rats. Methods: Twenty-eight male Wistar rats were divided into 4 groups of control, gentamicin (100 mg/kg), and gentamicin plus 50- and 100-mg/kg/day fucoidan pretreatment. In the end, all rats were killed, and then urine, blood, and tissue samples were prepared. Kidney weight (KW), body weight (BW), and 24-hour urine volume, as well as serum creatinine (Cr), blood urea nitrogen (BUN), Cr clearance, and malondialdehyde (MDA) levels and superoxide dismutase (SOD) activity, were measured. Kidney samples were also evaluated for histopathological changes. Results: Gentamicin significantly increased KW, KW/BW ratio, 24-hour urine volume, serum Cr, MDA, and BUN levels; however, fucoidan pretreatment, especially at a dose of 50 mg/kg, significantly returned these variables near to the control group values. Gentamicin also decreased BW gain, Cr clearance, SOD activity, and the degree of renal tissue damage compared to the control group, while treatment with fucoidan significantly reversed these alterations. Conclusions: The results show that fucoidan from S. angustifolium C. Agardh 1820 ameliorates gentamicin-induced nephrotoxicity by alleviating oxidative stress and augmenting antioxidant enzymes activity in renal tissue, suggesting the potential use of this fucoidan in a clinical setting.