Potassium starvation-induced oxidative stress and antioxidant defense responses in Brassica juncea

ABSTRACT Oxidative stresses commonly exist in natural environments, and microbes have developed a variety of defensive systems to counteract such events. Although increasing evidence has shown that high hydrostatic pressure (HHP) and low temperature (LT) induce antioxidant defense responses in cells, there is no direct evidence to prove the connection between antioxidant defense mechanisms and the adaptation of bacteria to HHP and LT. In this study, using the wild-type (WT) strain of a deep-sea bacterium, Shewanella piezotolerans WP3, as an ancestor, we obtained a mutant, OE100, with an enhanced antioxidant defense capacity by experimental evolution under H 2 O 2 stress. Notably, OE100 exhibited better tolerance not only to H 2 O 2 stress but also to HHP and LT (20 MPa and 4°C, respectively). Whole-genome sequencing identified a deletion mutation in the oxyR gene, which encodes the transcription factor that controls the oxidative stress response. Comparative transcriptome analysis showed that the genes associated with oxidative stress defense, anaerobic respiration, DNA repair, and the synthesis of flagella and bacteriophage were differentially expressed in OE100 compared with the WT at 20 MPa and 4°C. Genetic analysis of oxyR and ccpA2 indicated that the OxyR-regulated cytochrome c peroxidase CcpA2 significantly contributed to the adaptation of WP3 to HHP and LT. Taken together, these results confirmed the inherent relationship between antioxidant defense mechanisms and the adaptation of a benthic microorganism to HHP and LT. IMPORTANCE Oxidative stress exists in various niches, including the deep-sea ecosystem, which is an extreme environment with conditions of HHP and predominantly LT. Although previous studies have shown that HHP and LT induce antioxidant defense responses in cells, direct evidence to prove the connection between antioxidant defense mechanisms and the adaptation of bacteria to HHP and LT is lacking. In this work, using the deep-sea bacterium Shewanella piezotolerans WP3 as a model, we proved that enhancement of the adaptability of WP3 to HHP and LT can benefit from its antioxidant defense mechanism, which provided useful insight into the ecological roles of antioxidant genes in a benthic microorganism and contributed to an improved understanding of microbial adaptation strategies in deep-sea environments.

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Bamboo Leaf Flavonoids Extracts Alleviate Oxidative Stress in HepG2 Cells via Naturally Modulating Reactive Oxygen Species Production and Nrf2‐Mediated Antioxidant Defense Responses

Journal of Food Science ◽

10.1111/1750-3841.14609 ◽

2019 ◽

Vol 84 (6) ◽

pp. 1609-1620 ◽

Cited By ~ 10

Author(s):

Yue Yu ◽

Zhanming Li ◽

Guangtian Cao ◽

Shudan Huang ◽

Hongshun Yang

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Hepg2 Cells ◽

Reactive Oxygen Species Production ◽

Antioxidant Defense ◽

Reactive Oxygen ◽

Defense Responses ◽

Oxygen Species ◽

Species Production

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Role of Heme Oxygenase1 in Alteration of Antioxidant Defense Responses of Brassica Juncea (L.) Czern. under Salt Stress Condition

International Journal of Scientific Research in Environmental Sciences ◽

10.12983/ijsres-2015-p0119-0128 ◽

2015 ◽

Vol 3 (3) ◽

pp. 119-128

Author(s):

Khushbu Verma ◽

Afroz Alam

Keyword(s):

Salt Stress ◽

Brassica Juncea ◽

Antioxidant Defense ◽

Stress Condition ◽

Defense Responses ◽

Salt Stress Condition

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Oxidative stress and antioxidant defense responses in Acartia copepods in relation to environmental factors

PLoS ONE ◽

10.1371/journal.pone.0195981 ◽

2018 ◽

Vol 13 (4) ◽

pp. e0195981 ◽

Cited By ~ 14

Author(s):

Olivier Glippa ◽

Jonna Engström-Öst ◽

Mirella Kanerva ◽

Anni Rein ◽

Kristiina Vuori

Keyword(s):

Oxidative Stress ◽

Environmental Factors ◽

Antioxidant Defense ◽

Defense Responses

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Protective Effects of Sulforaphane on Exercise-Induced Organ Damage via Inducing Antioxidant Defense Responses

Antioxidants ◽

10.3390/antiox9020136 ◽

2020 ◽

Vol 9 (2) ◽

pp. 136 ◽

Cited By ~ 7

Author(s):

Ruheea Taskin Ruhee ◽

Sihui Ma ◽

Katsuhiko Suzuki

Keyword(s):

Oxidative Stress ◽

Mrna Expression ◽

Antioxidant Defense ◽

Defense Responses ◽

Organ Damage ◽

Exercise Group ◽

Exhaustive Exercise ◽

Protective Effects ◽

Antioxidant Defense Enzymes ◽

Exercise Induced

Regular exercise is beneficial to maintain a healthy lifestyle, but the beneficial effects are lost in the case of acute exhaustive exercise; this causes significant inflammation, oxidative stress along with organ damage. Recently, sulforaphane (SFN), an indirect antioxidant, has drawn special attention for its potential protective effect against inflammation and oxidative stress. However, no studies have been performed regarding acute exhaustive exercise-induced organ damage in association with SFN administration. Therefore, the aim of this study was to investigate the effects of SFN on acute exhaustive exercise-induced organ damage and the mechanisms involved. To perform the study, we divided mice into four groups: Control, SFN, exercise, and SFN plus exercise. The SFN group was administered orally (50 mg/kg body wt) 2 h before the running test. We measured plasma levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH), and acute exhaustive exercise significantly increased these biomarkers. In addition, the mRNA expression of pro-inflammatory cytokines, IL-6, IL-1β, and TNF-α, were significantly increased in the liver of exercise group. However, the SFN plus exercise group showed a significant reduction in the expression of cytokines and blood biomarkers of tissue damage or cell death. Furthermore, we measured mRNA expression of Nrf2, heme oxygenase (HO)-1, and antioxidant defense enzymes expression, i.e., superoxide dismutase (SOD1), catalase (CAT), and glutathione peroxidase (GPx1) in the liver. The expression of all these biomarkers was significantly upregulated in the SFN plus exercise group. Collectively, SFN may protect the liver from exhaustive exercise-induced inflammation via inducing antioxidant defense response through the activation of Nrf2/HO-1 signal transduction pathway.

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