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Microorganisms: A Potential Source of Bioactive Molecules for Antioxidant Applications - PubMed

  • ️Fri Jan 01 2021

Review

Microorganisms: A Potential Source of Bioactive Molecules for Antioxidant Applications

Alka Rani et al. Molecules. 2021.

Abstract

Oxidative stress originates from an elevated intracellular level of free oxygen radicals that cause lipid peroxidation, protein denaturation, DNA hydroxylation, and apoptosis, ultimately impairing cell viability. Antioxidants scavenge free radicals and reduce oxidative stress, which further helps to prevent cellular damage. Medicinal plants, fruits, and spices are the primary sources of antioxidants from time immemorial. In contrast to plants, microorganisms can be used as a source of antioxidants with the advantage of fast growth under controlled conditions. Further, microbe-based antioxidants are nontoxic, noncarcinogenic, and biodegradable as compared to synthetic antioxidants. The present review aims to summarize the current state of the research on the antioxidant activity of microorganisms including actinomycetes, bacteria, fungi, protozoa, microalgae, and yeast, which produce a variety of antioxidant compounds, i.e., carotenoids, polyphenols, vitamins, and sterol, etc. Special emphasis is given to the mechanisms and signaling pathways followed by antioxidants to scavenge Reactive Oxygen Species (ROS), especially for those antioxidant compounds that have been scarcely investigated so far.

Keywords: astaxanthin; microalgae; mycothiol; natural antioxidant; oxidative stress; peroxiredoxin.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1

Various sources of oxidative stress and antioxidants.

Figure 2
Figure 2

MSH biosynthesis and regulation in actinomycetes. Synthesis of MSH is catalyzed by five enzymes, including MshA, MshA2, MshB, MshC, and MshD. 1) Under Reactive Oxygen Species (ROS), MSH is oxidized to MSSM, which is further reduced by Mtr. 2) S-mycothiolation and protein regeneration occur via Mrx1 (mycoredoxin 1) /MSH/Mtr and thioredoxin/Thioredoxin reductase (Trx /TrxR) pathway. 3) Arsenate reductases CgArsC1/CgArsC2 along with MSH and Mrx1 reduced As (V) to As (III), which is exported through ABC transporter. 4) MSH acts as thiol cofactor for alcohol dehydrogenase MscR and formaldehyde dehydrogenase AdhE and is involved in NO and formaldehyde detoxification. 5) Mycothiol amidase (Mca) and mycothiol-S-transferases are involved in ROS and xenobiotic detoxification.

Figure 3
Figure 3

Probiotic activates metabolites and enzymes that enter the cell through toll-like receptors (TLR) and induced Nrf2-Keap1-ARE pathway. During ROS attack, the redox-sensitive cysteine residues of Keap1 react and disrupt the functional conformation of Keap1, thereby activating Nrf2. Nrf2 translocates towards the nucleus and binds to antioxidant response element (ARE) sequences, activating the transcription of ARE-driven genes, encoding antioxidant enzymes, and detoxifying proteins. ROS mediates the expression of redox-sensitive transcription factor NFκB and further expression of inflammatory cytokines. ROS also activates SIRT1 (Silent information regulator T1), mediated Adenosine monophosphate (AMP)-activated protein kinase (AMPK) pathway.

Figure 4
Figure 4

Two-step catalytic mechanism of 2-Cys Prx. The sulfhydryl group at the 2-Cys Prxs is oxidized to sulfenic acid (–SOH), which condenses with the –SH group at the cysteine from the other subunit forming an inter-subunit disulfide bond. This bond is further reduced by thioredoxin (Trx) or another reductase. Continuous peroxide signaling leads to reversible hyperoxidation and formation of sulfinic acid (–SOOH) at peroxidatic cysteine. Sulfinic 2-Cys Prx is reduced by sulfiredoxin (Srx) with an ATP’s consumption and generates a sulfinic phosphoryl ester intermediate. Cys 99 present in Srx reacts with this intermediate to form thiosulfinate that can be attacked by RSH to generate sulfenic acid. (RSH signifies a thiol equivalent such as glutathione, dithiothreitol, or thioredoxin). Adapted from [140].

Figure 5
Figure 5

Some antioxidant compounds reported from microalgae.

Figure 6
Figure 6

Mode of action of astaxanthin by inhibiting oxidative stress-induced mitochondrial dysfunction and activating transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2). Astaxanthin suppresses nuclear expression of NF-κB and MAPK to reduce downstream production of proinflammatory cytokines. NF-κB: Nuclear factor-κB; MMP: matrix metallopeptidase; MAPK: mitogen-activated protein kinase; ARE: Antioxidant response elements.

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