Relationship of Gene-Structure–Antioxidant Ability of Exopolysaccharides Derived from Lactic Acid Bacteria: A Review

Abstract

Polysaccharides derived from lactic acid bacteria (LAB) have widespread industrial applications owing to their excellent safety profile and numerous biological properties. The antioxidant activity of exopolysaccharides (EPS) offers defense against disease conditions caused by oxidative stress. Several genes and gene clusters are involved in the biosynthesis of EPS and the determination of their structures, which play an important role in modulating their antioxidant ability. Under conditions of oxidative stress, EPS are involved in the activation of the nonenzyme (Keap1-Nrf2-ARE) response pathway and enzyme antioxidant system. The antioxidant activity of EPS is further enhanced by the targeted alteration of their structures, as well as by chemical methods. Enzymatic modification is the most commonly used method, though physical and biomolecular methods are also frequently used. A detailed summary of the biosynthetic processes, antioxidant mechanisms, and modifications of LAB-derived EPS is presented in this paper, and their gene-structure−function relationship has also been explored.

Effect of modified okara insoluble dietary fibre on the quality of yoghurt

“…Adding dietary fibre can increase the number of microorganisms and the production of active substances. For example, extracellular polysaccharides secreted by lactic acid bacteria have good antioxidant effects ( Zhou et al, 2023 ). Notably, the antioxidant activity of yoghurt in the control group also slowly decreased during the storage period.…”

Lactic Acid Bacteria-Derived Exopolysaccharides Mitigate the Oxidative Response via the NRF2-KEAP1 Pathway in PC12 Cells

“…We believe that our L-EPS possess a number of different mechanisms of action in regards to their regulatory effect on TDH. These include the chelation of metal ions [44], the scavenging of free radicals [45], the formation of specific redox reaction (GSH) substrates [46], and specifically, the reduction of some different protein disulfate bonds (thioredoxin) [47]. However, further research is needed to fully understand the precise mechanism and clinical applications of the regulatory effect of our L-EPS on TDH.…”