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      Sesame meal and lemon zest – enriched mayonnaise: Proximal analysis and toxicological studies in animals

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          Abstract

          Considering the high global consumption of mayonnaise and modern concerns about the health value of food products, the recipe for mayonnaise sauces is constantly evolving. In this study, we present the proximal analysis and toxicological evaluation of a new mayonnaise, which was patented. Starch was replaced with sesame meal, and lemon zest was added as an antioxidant. Compared to a mayonnaise prepared using a traditional recipe as control, the enriched mayonnaise had higher protein and lower fat content, suggesting a potentially healthier product. Aditionally, peroxide and anisidine values were lower in the new mayonnaise, indicating higher resistance to oxidative damage. Toxicological studies of the enriched mayonnaise, including oral moderate-to-lethal dose (acute oral toxicity), cumulative (subacute) action, irritating effect on mucous membranes, and sensitizing properties, which were conducted on laboratory animals following required regulatory standards, are shown in this work. The patented sesame meal and lemon zest-enriched mayonnaise proved to be safe in all performed studies, meeting safety requirements regarding toxicological parameters. Furthermore, the enriched mayonnaise is affordable, with a production cost similar to that of control mayonnaise.

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          Highlights

          • Potentially healthier mayonnaise where starch and antioxidants were replaced with sesame meal and lemon zest was developed.

          • New mayonnaise has a higher protein and lesser fat amount than control, what may indicate a potentially healthier product.

          • AV and PV were lower in new mayonnaise than in control, which may indicate a higher resistance to oxidative damage.

          • No toxicological effects of the new mayonnaise were found.

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          Most cited references31

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          Phenolics and polyphenolics in foods, beverages and spices: Antioxidant activity and health effects – A review

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            The Probable Error of a Mean

            Student (1908)
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              The Evidence for Saturated Fat and for Sugar Related to Coronary Heart Disease.

              Dietary guidelines continue to recommend restricting intake of saturated fats. This recommendation follows largely from the observation that saturated fats can raise levels of total serum cholesterol (TC), thereby putatively increasing the risk of atherosclerotic coronary heart disease (CHD). However, TC is only modestly associated with CHD, and more important than the total level of cholesterol in the blood may be the number and size of low-density lipoprotein (LDL) particles that contain it. As for saturated fats, these fats are a diverse class of compounds; different fats may have different effects on LDL and on broader CHD risk based on the specific saturated fatty acids (SFAs) they contain. Importantly, though, people eat foods, not isolated fatty acids. Some food sources of SFAs may pose no risk for CHD or possibly even be protective. Advice to reduce saturated fat in the diet without regard to nuances about LDL, SFAs, or dietary sources could actually increase people's risk of CHD. When saturated fats are replaced with refined carbohydrates, and specifically with added sugars (like sucrose or high fructose corn syrup), the end result is not favorable for heart health. Such replacement leads to changes in LDL, high-density lipoprotein (HDL), and triglycerides that may increase the risk of CHD. Additionally, diets high in sugar may induce many other abnormalities associated with elevated CHD risk, including elevated levels of glucose, insulin, and uric acid, impaired glucose tolerance, insulin and leptin resistance, non-alcoholic fatty liver disease, and altered platelet function. A diet high in added sugars has been found to cause a 3-fold increased risk of death due to cardiovascular disease, but sugars, like saturated fats, are a diverse class of compounds. The monosaccharide, fructose, and fructose-containing sweeteners (e.g., sucrose) produce greater degrees of metabolic abnormalities than does glucose (either isolated as a monomer, or in chains as starch) and may present greater risk of CHD. This paper reviews the evidence linking saturated fats and sugars to CHD, and concludes that the latter is more of a problem than the former. Dietary guidelines should shift focus away from reducing saturated fat, and from replacing saturated fat with carbohydrates, specifically when these carbohydrates are refined. To reduce the burden of CHD, guidelines should focus particularly on reducing intake of concentrated sugars, specifically the fructose-containing sugars like sucrose and high-fructose corn syrup in the form of ultra-processed foods and beverages.
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                Author and article information

                Contributors
                Journal
                Heliyon
                Heliyon
                Heliyon
                Elsevier
                2405-8440
                18 March 2024
                30 March 2024
                18 March 2024
                : 10
                : 6
                : e28319
                Affiliations
                [1]Food Products Technology Department, Food Products Technology Faculty, Tashkent Institute of Chemical Technology, Tashkent City, Uzbekistan
                Author notes
                [* ]Corresponding author. charosgaipova@ 123456gmail.com
                Article
                S2405-8440(24)04350-0 e28319
                10.1016/j.heliyon.2024.e28319
                10965816
                38545223
                99527f56-d52c-46b0-ab73-9d792ae8a96b
                © 2024 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 28 June 2023
                : 14 March 2024
                : 15 March 2024
                Categories
                Research Article

                mayonnaise,sesame meal,toxicology,toxicological evaluation

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