4.7 Article

Food-grade lactic acid bacteria and probiotics as a potential protective tool against erythrotoxic dietary xenobiotics

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TRENDS IN FOOD SCIENCE & TECHNOLOGY
卷 116, 期 -, 页码 1041-1055

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ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tifs.2021.09.004

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  1. National Council for Science and Technology (CONACYT) of Mexico

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Food-grade lactic acid bacteria and probiotics, as well as their metabolites, have shown potential in protecting erythrocytes from oxidative damage induced by dietary xenobiotics. They can enhance the antioxidant system of erythrocytes, improve the bioavailability of antioxidants, and increase the expression of antioxidant enzymes in the host, providing a new approach to counteract oxidative stress.
Background: Different studies have evidenced that dietary xenobiotics (DXBs) can produce oxidative damage to erythrocytes, which eventually leads to the development of eryptosis and, ultimately hemolysis. Increased eryptosis and hemolysis have been implicated in the development and progression of some clinical conditions or chronic diseases, mainly from cardiovascular origin. Therefore, new strategies based on agents with antioxidant properties have emerged as a novel approach to reduce induced oxidative stress in exposed erythrocytes. Scope and approach: Specific food-grade lactic acid bacteria and probiotics have exhibited antioxidant properties, likely related to postbiotics, with positive effects against oxidative damage in human erythrocytes. Hence, the aim of this work was to provide an overview of the current knowledge regarding the possible protective role of food-grade LAB and/or probiotics, as well as their metabolites (postbiotics), against the erythrotoxic effect induced by DXBs. The possible mechanisms underlying this protective activity will also be described. Key findings and conclusions: In vitro and in vivo studies have shown that food-grade lactic acid bacteria and/or probiotics have the capacity to improve the enzymatic and non-enzymatic antioxidant system of erythrocytes, thereby exhibiting protection against induced-oxidative damage by DXBs. The possible mechanisms involve the enhancement of the bioaccessibility of exogenous antioxidant precursor molecules and/or the bioavailability of endogenous antioxidants. Besides, the increased expression of genes that codify for the production of antioxidant enzymes in the host, induced by bacteria-derived byproducts, is not ruled out.

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