Postharvest Application of Acibenzolar-S-methyl Delays the Senescence of Pear Fruit by Regulating Reactive Oxygen Species and Fatty Acid Metabolism

2020 ◽  
Vol 68 (17) ◽  
pp. 4991-4999 ◽  
Author(s):  
Xue Li ◽  
Canying Li ◽  
Yuan Cheng ◽  
Jiabao Hou ◽  
Junhu Zhang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Fatty Acid ◽  
Fatty Acid Metabolism ◽  
Acid Metabolism ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Pear Fruit ◽  
Postharvest Application

scholarly journals Herbivore-derived fatty-acid amides elicit reactive oxygen species burst in plants

2017 ◽  
Vol 69 (5) ◽  
pp. 1235-1245 ◽  
Author(s):  
Anna Block ◽  
Shawn A Christensen ◽  
Charles T Hunter ◽  
Hans T Alborn
Keyword(s):  
Reactive Oxygen Species ◽  
Fatty Acid ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Fatty Acid Amides ◽  
Reactive Oxygen Species Burst

scholarly journals Non-esterified Fatty Acid-Induced Reactive Oxygen Species Mediated Granulosa Cells Apoptosis Is Regulated by Nrf2/p53 Signaling Pathway

Antioxidants ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 523
Author(s):  
Yiru Wang ◽  
Chengmin Li ◽  
Julang Li ◽  
Genlin Wang ◽  
Lian Li
Keyword(s):  
Reactive Oxygen Species ◽  
Fatty Acid ◽  
Granulosa Cells ◽  
Ovarian Function ◽  
Reactive Oxygen ◽  
Follicular Development ◽  
Oxygen Species ◽  
Related Protein ◽  
Induced Apoptosis

Negative energy balance (NEB) during the perinatal period can affect dairy cow follicular development and reduce the fecundity. Non-esterified fatty acid (NEFA) concentration is elevated during NEB, and is known to be toxic for multiple cell types. In the ovary, NEB increased NEFA, and may influences follicular growth and development. However, the effect and mechanism of NEFA on granulosa cells (GCs) in vitro remains unknown. In this study, we found that NEFA dose-dependently induced apoptosis in primary cultured granulosa cells. Mechanistically, our data showed that NEFA significantly increased reactive oxygen species (ROS) levels, resulting in the activation of endoplasmic reticulum stress (ERS) and eventually cell apoptosis in GCs. Moreover, NEFA also increased the phosphorylation levels of ERK1/2 and p38MAPK pathways, upregulated the expression of p53 and potentially promoted its translocation to the nuclear, thus transcriptionally activated Bax, a downstream gene of this pathway. NEFA also promoted nuclear factor E2 (Nrf2) expression and its level in the nuclear. To elucidate the mechanism of NEFA action, N-acetyl-l-cysteine (NAC), a ROS scavenger was used to verify the role of ROS in NEFA induced apoptosis of GCs. NAC pretreatment reversed the NEFA-induced ERS-related protein and apoptosis-related protein levels. Meanwhile, NAC pretreatment also blocked the phosphorylation of ERK1/2 and p38 induced by NEFA, and the nucleation of Nrf2 and p53, suggesting that ROS plays a crucial role in regulating the NEFA-induced apoptosis of GCs. Together, these findings provide an improved understanding of the mechanisms underlying GCs apoptosis, which could potentially be useful for improving ovarian function.

scholarly journals Production of reactive oxygen species by PuRBOHF is critical for stone cell development in pear fruit

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Xiaoqian Wang ◽  
Siqi Liu ◽  
Huili Sun ◽  
Chunyan Liu ◽  
Xinyue Li ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Formation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Pear Fruit ◽  
Specific Expression ◽  
Stone Cell ◽  
Transient Overexpression ◽  
Microscopy Data ◽  
Respiratory Burst Oxidase

AbstractThe production of reactive oxygen species (ROS) by NADPH oxidase, which is also referred to as respiratory burst oxidase homolog (RBOH), affects several processes in plants. However, the role of RBOHs in cell wall lignification is not well understood. In this study, we show that PuRBOHF, an RBOH isoform, plays an important role in secondary wall formation in pear stone cells. ROS were closely associated with lignin deposition and stone cell formation according to microscopy data. In addition, according to the results of an in situ hybridization analysis, the stage-specific expression of PuRBOHF was higher in stone cells than in cells of other flesh tissues. Inhibitors of RBOH activity suppressed ROS accumulation and stone cell lignification in pear fruit. Moreover, transient overexpression of PuRBOHF caused significant changes in the amount of ROS and lignin that accumulated in pear fruit and flesh calli. We further showed that PuMYB169 regulates PuRBOHF expression, while PuRBOHF-derived ROS induces the transcription of PuPOD2 and PuLAC2. The findings of this study indicate that PuRBOHF-mediated ROS production, which is regulated by a lignin-related transcriptional network, is essential for monolignol polymerization and stone cell formation in pear fruit.

Role of mitochondrial complexes I and II, reactive oxygen species and arachidonic acid metabolism in deoxycholate-induced apoptosis

2002 ◽  
Vol 177 (2) ◽  
pp. 129-144 ◽  
Author(s):  
Delon Washo-Stultz ◽  
Cara L Crowley-Weber ◽  
Katerina Dvorakova ◽  
Carol Bernstein ◽  
Harris Bernstein ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Arachidonic Acid ◽  
Acid Metabolism ◽  
Reactive Oxygen ◽  
Arachidonic Acid Metabolism ◽  
Oxygen Species ◽  
Mitochondrial Complexes ◽  
Induced Apoptosis

scholarly journals Inhibition of Fatty Acid Oxidation Promotes Macrophage Control of Mycobacterium tuberculosis

mBio ◽  
2020 ◽  
Vol 11 (4) ◽  
Author(s):  
Pallavi Chandra ◽  
Li He ◽  
Matthew Zimmerman ◽  
Guozhe Yang ◽  
Stefan Köster ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Mycobacterium Tuberculosis ◽  
Fatty Acid ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Metabolic Reprogramming ◽  
Acid Oxidation ◽  
Oxygen Species ◽  
Content Type ◽  
Mitochondrial Fatty Acid

ABSTRACT Macrophage activation involves metabolic reprogramming to support antimicrobial cellular functions. How these metabolic shifts influence the outcome of infection by intracellular pathogens remains incompletely understood. Mycobacterium tuberculosis (Mtb) modulates host metabolic pathways and utilizes host nutrients, including cholesterol and fatty acids, to survive within macrophages. We found that intracellular growth of Mtb depends on host fatty acid catabolism: when host fatty acid β-oxidation (FAO) was blocked chemically with trimetazidine, a compound in clinical use, or genetically by deletion of the mitochondrial fatty acid transporter carnitine palmitoyltransferase 2 (CPT2), Mtb failed to grow in macrophages, and its growth was attenuated in mice. Mechanistic studies support a model in which inhibition of FAO generates mitochondrial reactive oxygen species, which enhance macrophage NADPH oxidase and xenophagy activity to better control Mtb infection. Thus, FAO inhibition promotes key antimicrobial functions of macrophages and overcomes immune evasion mechanisms of Mtb. IMPORTANCE Mycobacterium tuberculosis (Mtb) is the leading infectious disease killer worldwide. We discovered that intracellular Mtb fails to grow in macrophages in which fatty acid β-oxidation (FAO) is blocked. Macrophages treated with FAO inhibitors rapidly generate a burst of mitochondria-derived reactive oxygen species, which promotes NADPH oxidase recruitment and autophagy to limit the growth of Mtb. Furthermore, we demonstrate the ability of trimetazidine to reduce pathogen burden in mice infected with Mtb. These studies will add to the knowledge of how host metabolism modulates Mtb infection outcomes.

Sign in / Sign up

Export Citation Format

Share Document