The quality of commercial fish oil products can be difficult to maintain because of the rapid lipid oxidation attributable to the high number of polyunsaturated fatty acids (PUFA), specifically eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). While it is known that oxidation in fish oil is generally the result of a direct interaction with oxygen and fatty acid radicals, there are very few studies that investigate the oxidation kinetics of fish oil supplements. This study uses hydroperoxides, a primary oxidation product, to model the oxidation kinetics of two commercially available fish oil supplements with different EPA and DHA contents. Pseudo first order kinetics were assumed, and rate constants were determined for temperatures between 4 and 60 °C. This data was fit to the Arrhenius model, and activation energies (E(a)) were determined for each sample. Both E(a) agreed with values found in the literature, with the lower PUFA sample having a lower E(a). The oil with a lower PUFA content fit the first-order kinetics model at temperatures ≥20 °C and ≤40 °C, while the higher PUFA oil demonstrated first-order kinetics at temperatures ≥4 °C and ≤40 °C. When the temperature was raised to 60 °C, the model no longer applied. This indicates that accelerated testing of fish oil should be conducted at temperatures ≤40 °C.

The long-chain polyunsaturated fatty acids (PUFA) found in fish oil, specifically eicosapentanoic acid (EPA) and docosahexanoic acid (DHA) play an important part in human health. As a result, fish oil supplements are commonly consumed by people around the world. Supplements in the form of triacylglycerols (TAG) can be sold at a premium price, compared to those in the ethyl ester (EE) forms. Producers of TAG supplements require a simple, rapid method to determine the authenticity of their raw material. Here, we describe a method to quantify EE in fish oil using solid phase microextraction headspace analysis and GCMS. Despite the variation in linear ranges of the calibration curves with volatility of the EE, 30 individual FA were quantified including common saturated FA such as palmitic and stearic acid, as well as longer chain PUFA, such as EPA and DHA. The method was then applied to three commercial fish oils in the TAG form and two of the products were found to contain EE, with one containing EE above 1.5% w/w, indicating that contamination had occurred. With growing consumer interest in fish oil products, the method proposed here will help resolve future issues of authenticity in fish oils.

Summary Background/purpose Sunburn and other health risks associated with excess sun exposure place huge economic burdens on societies, and create discomfort and disease within susceptible individuals. Oral supplements that reduce sunburn may be advantageous. This study evaluated the safety and efficacy of Bend Skincare Anti‐Aging Formula to ameliorate sunburn induced with a solar simulator. Methods Subjects (n = 28) with Fitzpatrick skin phototypes I, II, or III took 4 capsules daily of the supplement providing 1400 mg of eicosapentaenoic acid (EPA) + docosahexaenoic acid (DHA), 120 mg of gamma‐linolenic acid (GLA), 5 mg of lutein, 2.5 mg of zeaxanthin, and 1000 IU of vitamin D3 for 8 weeks. Skin on each subject's back was exposed to a progressive sequence of timed ultraviolet (UV) radiation exposure doses at baseline, and after 4‐ and 8‐week treatment to determine their minimal erythema dose (MED). Results were compared before and after treatment using 3 paired t tests and subsequently 3 linear mixed models. Results Treatment significantly improved tolerance to UV exposure as evidenced by increased MED at 4 and 8 weeks compared with baseline (P < .001). This protection increased with prolonged use of Bend Skincare Anti‐Aging Formula as demonstrated by progressively increased MED between baseline and 4 weeks, and again between 4 and 8 weeks (P < .001). Nearly 86% of patients responded to treatment within 4 weeks and 100% of patients responded by the end of the study, resulting in a 39% mean increase in MED at 4 weeks, and an 84% mean increase in MED at 8 weeks compared with baseline. Treatment was well tolerated with no product associated adverse events (AE) and only a few mild and expected side effects. Conclusion Bend Skincare Anti‐Aging Formula safely and effectively provides significant skin photoprotection that increases with continued use.

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BackgroundOverexposure to ultraviolet (UV) light is associated with multiple health risks from sunburn to skin cancers. The ingestion of natural product photoprotectors can increase skin's UV‐resistance. Our research focuses on the cellular effects of Bend Beauty, Inc.'s oral supplement called “Bend Skincare Anti‐Aging Formula” (AAF), which contains daily doses of the ω‐3 fatty acids eicosapentaenoic acid (EPA; 1050 mg) and docosahexaenoic acid (DHA; 350 mg), ω‐6 fatty acid gamma‐linolenic acid (GLA; 120 mg), carotenoids zeaxanthin (2.5 mg) and lutein (5 mg), and vitamin D3 (1,000 IU). A clinical trial found that ingestion of AAF increased the minimal erythema doses (UV exposure required to induce skin redness) of volunteers' skin by 84% after 8 weeks, warranting further research into AAF's photoprotective properties.ObjectiveTo quantify AAF's photoprotective and antioxidant properties in human dermal fibroblasts.Methods & ResultsExperiments were completed in primary human dermal fibroblasts (passage #3) treated with 0.005% AAF or vehicle control (10% H2O, 10% THF, 75% DMSO, 5% FBS). For the initial photoprotection assays, cells were treated with AAF or vehicle for 1, 7, or 14 days and exposed to UVA (365 nm; 216 J/cm2) or UVB (312 nm; 15.6 – 8,000 J/cm2). The viability of 1, 7, and 14‐day AAF‐treated cells after UVA exposure was 2.9, 4.2, and 3.5‐fold higher, respectively, vs. control (P < 0.05), and the UVB IC50s were 2.6 and 3.2‐fold higher in 7 and 14‐day AAF‐treated cells, respectively, vs. control (P < 0.05) as measured with MTT assays. For morphological analysis, 14‐day AAF‐ or vehicle‐treated fibroblasts were exposed to UVA (100 J/cm2) or UVB (1 J/cm2), stained with propidium iodide (PI; cell death marker), phalloidin (cytoskeleton stain), and Hoechst 32258 (nucleic stain) and imaged using confocal microscopy. After UVA or UVB exposure, the vehicle‐treated cells were visibly more damaged than AAF‐treated cells as assessed by actin staining, and PI staining was present in > 97% of the vehicle‐treated vs. < 8% of AAF‐treated fibroblasts (Figure 1). To quantify AAF's antioxidant effects, MTT assays were completed in 1, 7, and 14‐day AAF‐treated fibroblasts after 48 hours of treatment with the reactive oxygen species (ROS), H2O2 (11.1 – 2,700 mM); H2O2's IC50 values were calculated to be 2.0, 2.4, and 2.5‐fold higher, respectively, vs. control (P < 0.05). In identically AAF‐treated fibroblasts, assays to measure the intracellular ROS activity induced by H2O2 (0.9 mM, 1 h) using a ROS‐fluorescent probe (CM‐DCFH2‐DA) were completed. H2O‐2‐induced ROS activity was 67%, 63%, and 62% as high in 1, 7, and 14‐day AAF‐treated cells vs. control, respectively (P < 0.05).ConclusionsAAF helps to protect human dermal fibroblasts from the damaging effects of UVA, UVB, and H2O2, demonstrating its cellular photoprotective and antioxidant properties.Support or Funding InformationProject funding provided by Bend Beauty, Inc., Mitacs Elevate, and the Dalhousie Pharmacy Endowment FundThis abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.