scholarly journals Influence of PM2.5 on spermatogenesis dysfunction via the reactive-oxygen-species-mediated Mitogen-activated-protein-kinase signaling pathway

2019 ◽  
Vol 6 (4) ◽  
pp. 77-79
Author(s):  
Ruangrong Cheepsattayakorn
Keyword(s):  
Reactive Oxygen Species ◽  
Signaling Pathway ◽  
Reactive Oxygen ◽  
Human Sperm ◽  
Mapk Signaling ◽  
Autoimmune Response ◽  
Sperm Chromatin ◽  
Seminiferous Tubules ◽  
Oxygen Species ◽  
Mitogen Activated Protein

Approximately 15 % of the world‘s couples confront childless, and about 50 % of them are due to male reproductive disorders. Several previous studies demonstrated that PM2.5 particles has been consistently associated with critical human sperm reduction and impairment of human sperm chromatin and DNA from traffic exhaust pollution. Blood-testis barrier (BTB), a critically physical barrier between the seminiferous tubules and the blood vessels prevents sperm antigens from entering the blood circulation and facilitating and initiating an autoimmune response that contributing to spermatogenesis interference. Reactive oxygen species (ROS) are involved in the redox-sensitive signal transduction factors activation, such as Jun NH2-terminal kinase (JNK), p 38, extracellular signal-regulated kinase (ERK), and mitogen-activated protein kinases (MAPK) that critically influence BTB disruption. After PM2.5 exposure, there are decreased superoxide dismutase (SOD) expression, increased malondialdehyde (MDA) expression, increased nuclear factor erythroid 2-related factor 2 (Nrf-2) expression, increased expression of the four junctional proteins (β-catenin, Cx43, occludin, zonula occludens-1 (ZO-1)), thus improve sperm quality and quantity. PM2.5 particles markedly induce increasing phosphorylation of MAPKs via the ROS-mediated MAPK signaling pathway that causes BTB disruption, but this effect is lesser in the vitamins C and E intervention as well as increasing cleaved caspase-3 expression and the Bcl-2/Bax ratio. In conclusion, combined therapeutic administration of vitamins C and E can maintain the BTB integrity, reduce oxidative stress and cell apoptosis, and prevent toxic effects.

scholarly journals Mitogen-Activated Protein Kinases and Reactive Oxygen Species: How Can ROS Activate MAPK Pathways?

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Yong Son ◽  
Yong-Kwan Cheong ◽  
Nam-Ho Kim ◽  
Hun-Taeg Chung ◽  
Dae Gill Kang ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Protein Kinases ◽  
Reactive Oxygen ◽  
Mapk Signaling ◽  
Oxygen Species ◽  
Mitogen Activated Protein Kinases ◽  
Mapk Kinase ◽  
Mapk Pathways ◽  
Mitogen Activated Protein ◽  
P38 Mapks

Mitogen-activated protein kinases (MAPKs) are serine-threonine protein kinases that play the major role in signal transduction from the cell surface to the nucleus. MAPKs, which consist of growth factor-regulated extracellular signal-related kinases (ERKs), and the stress-activated MAPKs, c-jun NH2-terminal kinases (JNKs) and p38 MAPKs, are part of a three-kinase signaling module composed of the MAPK, an MAPK kinase (MAP2K) and an MAPK kinase (MAP3K). MAP3Ks phosphorylate MAP2Ks, which in turn activate MAPKs. MAPK phosphatases (MKPs), which recognize the TXY amino acid motif present in MAPKs, dephosphorylate and deactivate MAPKs. MAPK pathways are known to be influenced not only by receptor ligand interactions, but also by different stressors placed on the cell. One type of stress that induces potential activation of MAPK pathways is the oxidative stress caused by reactive oxygen species (ROS). Generally, increased ROS production in a cell leads to the activation of ERKs, JNKs, or p38 MAPKs, but the mechanisms by which ROS can activate these kinases are unclear. Oxidative modifications of MAPK signaling proteins and inactivation and/or degradation of MKPs may provide the plausible mechanisms for activation of MAPK pathways by ROS, which will be reviewed in this paper.

scholarly journals Reactive oxygen species rescue regeneration after silencing the MAPK–ERK signaling pathway in Schmidtea mediterranea

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
V. Jaenen ◽  
S. Fraguas ◽  
K. Bijnens ◽  
M. Heleven ◽  
T. Artois ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Signaling Pathway ◽  
Reactive Oxygen ◽  
Light Therapy ◽  
Erk Signaling ◽  
Model Organisms ◽  
Ros Production ◽  
Oxygen Species ◽  
Planarian Regeneration ◽  
Egfr Signaling Pathway

AbstractDespite extensive research on molecular pathways controlling the process of regeneration in model organisms, little is known about the actual initiation signals necessary to induce regeneration. Recently, the activation of ERK signaling has been shown to be required to initiate regeneration in planarians. However, how ERK signaling is activated remains unknown. Reactive Oxygen Species (ROS) are well-known early signals necessary for regeneration in several models, including planarians. Still, the probable interplay between ROS and MAPK/ERK has not yet been described. Here, by interfering with major mediators (ROS, EGFR and MAPK/ERK), we were able to identify wound-induced ROS, and specifically H2O2, as upstream cues in the activation of regeneration. Our data demonstrate new relationships between regeneration-related ROS production and MAPK/ERK activation at the earliest regeneration stages, as well as the involvement of the EGFR-signaling pathway. Our results suggest that (1) ROS and/or H2O2 have the potential to rescue regeneration after MEK-inhibition, either by H2O2-treatment or light therapy, (2) ROS and/or H2O2 are required for the activation of MAPK/ERK signaling pathway, (3) the EGFR pathway can mediate ROS production and the activation of MAPK/ERK during planarian regeneration.

scholarly journals Protective Effects of Gintonin on Reactive Oxygen Species-Induced HT22 Cell Damages: Involvement of LPA1 Receptor-BDNF-AKT Signaling Pathway

Molecules ◽  
2021 ◽  
Vol 26 (14) ◽  
pp. 4138
Author(s):  
Yeon-Jin Cho ◽  
Sun-Hye Choi ◽  
Ra-Mi Lee ◽  
Han-Sung Cho ◽  
Hyewhon Rhim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Signaling Pathway ◽  
Reactive Oxygen ◽  
Akt Signaling ◽  
Atp Depletion ◽  
Oxygen Species ◽  
Akt Signaling Pathway ◽  
Neuroprotective Effects ◽  
Lpa1 Receptor

Gintonin is a kind of ginseng-derived glycolipoprotein that acts as an exogenous LPA receptor ligand. Gintonin has in vitro and in vivo neuroprotective effects; however, little is known about the cellular mechanisms underlying the neuroprotection. In the present study, we aimed to clarify how gintonin attenuates iodoacetic acid (IAA)-induced oxidative stress. The mouse hippocampal cell line HT22 was used. Gintonin treatment significantly attenuated IAA-induced reactive oxygen species (ROS) overproduction, ATP depletion, and cell death. However, treatment with Ki16425, an LPA1/3 receptor antagonist, suppressed the neuroprotective effects of gintonin. Gintonin elicited [Ca2⁺]i transients in HT22 cells. Gintonin-mediated [Ca2⁺]i transients through the LPA1 receptor-PLC-IP3 signaling pathway were coupled to increase both the expression and release of BDNF. The released BDNF activated the TrkB receptor. Induction of TrkB phosphorylation was further linked to Akt activation. Phosphorylated Akt reduced IAA-induced oxidative stress and increased cell survival. Our results indicate that gintonin attenuated IAA-induced oxidative stress in neuronal cells by activating the LPA1 receptor-BDNF-TrkB-Akt signaling pathway. One of the gintonin-mediated neuroprotective effects may be achieved via anti-oxidative stress in nervous systems.

scholarly journals Defining the Mechanisms by Which the Reactive Oxygen Species By-Product, 4-Hydroxynonenal, Affects Human Sperm Cell Function1

2015 ◽  
Vol 92 (4) ◽  
Author(s):  
Mark A. Baker ◽  
Anita Weinberg ◽  
Louise Hetherington ◽  
Ana-Izabel Villaverde ◽  
Tony Velkov ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Sperm Cell ◽  
Reactive Oxygen ◽  
Human Sperm ◽  
Oxygen Species
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