Effects of hypoxic stress and recovery on oxidative stress, apoptosis, and intestinal microorganisms in Pelteobagrus vachelli

Aquaculture ◽  
2021 ◽  
pp. 736945
Author(s):  
Xiang Zheng ◽  
Dongyong Fu ◽  
Jinghao Cheng ◽  
Rongye Tang ◽  
Mingxu Chu ◽  
...  
2012 ◽  
Vol 24 (1) ◽  
pp. 153 ◽  
Author(s):  
E. B. Jeung ◽  
H. Yang

Preeclampsia is a pregnancy-specific disease characterised by de novo development of concurrent hypertension, proteinuria and oxidative stress in the placenta. In the placenta, intervillous blood flow increases after 10 weeks of gestation and results in exposure of trophoblast cells to oxygen. Hypoxia occurs during the development of placenta in the first trimester and is implicated in trophoblast differentiation. Ca2+ is a universal intracellular second messenger involved in many processes such as signal transduction, hormone secretion and programmed cell death. Human placental primary cell cultures were established from first-trimester human placentas (at 7 to 12 weeks of gestation). In this study, calcium-related proteins (CRPs; TRPV6, PMCA1, NCKX3 and CaBP-28k) were investigated at normoxia (5% CO2 in 95% air) or hypoxia (2% O2/93% N2/5%CO2) for 12 h in human placental cell line (BeWo) and human placental primary cell (hPC). We confirmed mRNA expression by real-time PCR and protein expression by Western blot analysis. The data were 2 or 3 individual experiments with triplicate samples and analysed by one-way ANOVA using Tukey's multiple comparison test. In hypoxia, the level of TRPV6 mRNA and protein was not changed, however, calcium transporters' (NCKX3, CaBP-28k) mRNA and protein expressions were significantly increased in hypoxic BeWo cell compared with control (normoxia). In addition, expression of PMCA1 mRNA and protein was decreased in hypoxic BeWo cells. In hPC, CRPs (TRPV6, PMCA1, NCKX3 and CaBP-28k) mRNA and protein expressions were significantly induced by hypoxic stress compared with control. These results, taken together, indicate that alterations of calcium transporters in hypoxic stress may be involved in calcium transport in the placenta and protection of the placental trophoblasts from the oxidative stress during the pregnancy.


Chemosphere ◽  
2016 ◽  
Vol 151 ◽  
pp. 271-279 ◽  
Author(s):  
Guosong Zhang ◽  
Jianqiang Mao ◽  
Fenfei Liang ◽  
Jiawei Chen ◽  
Cheng Zhao ◽  
...  

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 684-684
Author(s):  
Raul Castro-Portuguez ◽  
Jeremy Meyers ◽  
Sam Freitas ◽  
Hope Dang ◽  
Emily Turner ◽  
...  

Abstract Aging is characterized by a progressive decline in the normal physiological functions of an organism, ultimately leading to mortality. Metabolic changes throughout the aging process disrupt the balance and homeostasis of the cell. The kynurenine metabolic pathway is the sole de novo biosynthetic pathway for producing NAD+ from ingested tryptophan. Altered kynurenine pathway activity is associated with both aging and a variety of age-associated diseases, and kynurenine-based interventions can extend lifespan in Caenorhabditis elegans. Our laboratory recently demonstrated knockdown of the kynurenine pathway enzymes kynureninase (KYNU) or 3-hydroxyanthranilic acid dioxygenase (HAAO) increases lifespan by 20-30% in C elegans. However, the mechanism of how these interventions may modulate response against different stressors during the aging process has yet to be explored. Fluorescent reporter strains show the stress-responsive transcription factors skn-1 (ortholog of NRF2/NFE2L2; oxidative stress response) and hif-1 (ortholog of HIF1A; hypoxic stress response) to be highly upregulated when the kynurenine pathway is inhibited. We also demonstrated the increase expression of gst-4 and gcs-1 (transcriptional targets skn-1), which are involved in production of the antioxidant glutathione (GSH), as well as upregulation of cysl-2 (transcriptional target of hif-1), a regulator of cysteine biosynthesis from serine. We hypothesize that lifespan extension resulting from kynurenine pathway inhibition is mediated, at least in part, by upregulation of these transcription factors, providing elevated defense against oxidative stress and hypoxic stress.


2018 ◽  
Vol 2018 ◽  
pp. 1-19 ◽  
Author(s):  
Andrew J. O’Leary ◽  
Sarah E. Drummond ◽  
Deirdre Edge ◽  
Ken D. O’Halloran

Oxygen deficit (hypoxia) is a major feature of cardiorespiratory diseases characterized by diaphragm dysfunction, yet the putative role of hypoxic stress as a driver of diaphragm dysfunction is understudied. We explored the cellular and functional consequences of sustained hypoxic stress in a mouse model. Adult male mice were exposed to 8 hours of normoxia, or hypoxia (FiO2 = 0.10) with or without antioxidant pretreatment (N-acetyl cysteine, 200 mg/kg i.p.). Ventilation and metabolism were measured. Diaphragm muscle contractile function, myofibre size and distribution, gene expression, protein signalling cascades, and oxidative stress (TBARS) were determined. Hypoxia caused pronounced diaphragm muscle weakness, unrelated to increased respiratory muscle work. Hypoxia increased diaphragm HIF-1α protein content and activated MAPK, mTOR, Akt, and FoxO3a signalling pathways, largely favouring protein synthesis. Hypoxia increased diaphragm lipid peroxidation, indicative of oxidative stress. FoxO3 and MuRF-1 gene expression were increased. Diaphragm 20S proteasome activity and muscle fibre size and distribution were unaffected by acute hypoxia. Pretreatment with N-acetyl cysteine substantially enhanced cell survival signalling, prevented hypoxia-induced diaphragm oxidative stress, and prevented hypoxia-induced diaphragm dysfunction. Hypoxia is a potent driver of diaphragm weakness, causing myofibre dysfunction without attendant atrophy. N-acetyl cysteine protects the hypoxic diaphragm and may have application as a potential adjunctive therapy.


2013 ◽  
Vol 25 (1) ◽  
pp. 197
Author(s):  
H. Yang ◽  
E. B. Jeung

Preeclampsia is a pregnancy-specific disease characterized by the de novo development of concurrent hypertension, proteinuria, and oxidative stress in placenta. Hypoxia occurs during the development of placenta in the first trimester and is implicated in trophoblast differentiation. Oxidative stress, resulting from deficient remodeling of spiral arteries, is an important inducer of preeclampsia. The potassium-dependent sodium/calcium exchangers including NCKX3 and NCX1 play critical roles in the transport of intracellular calcium that is exchanged with extracellular sodium ions. Calcium-related proteins, NCXs, calbindin, calcium pumping proteins (TRPV5-6, PMCA1b), transcripts are abundant in the smooth muscle, uterus, aorta, and intestine. The expressions of calcium-related proteins in the kidney, duodenum, and placenta after hypoxic stress in rats at gestation Day 19.5 (GD 19.5) were examined by real-time PCR and Western blot analysis. Hypoxic condition did not change fetal weight; however, it significantly increased the weight of placenta compared to normoxic condition. In GD 19.5, renal NCKX3 and TRPV6 expressions were increased, whereas the levels of NCX1 were decreased in hypoxic rats compared with normoxic pregnant rats. The expressions of CaBP-9k, TRPV5, and PMCA1b were not altered in normoxic or hypoxic rat tissues. Duodenal expressions of CaBP-9k, TRPV5-6, and PMCA1 were decreased in hypoxic rats, whereas NCXs were not changed. The transcripts of NCKX3, TRPV5-6, and PMCA1b were highly expressed in the placenta of hypoxic rat. Taken together, the expressions of renal, duodenal, and placental calcium-related proteins appear to be modulated by hypoxia-induced oxidative stress, implying that calcium-related proteins may be involved in preeclamptic oxidative stress.


2013 ◽  
Vol 36 (11) ◽  
pp. 934-939 ◽  
Author(s):  
Satoshi Nishioka ◽  
Toshitaka Yoshioka ◽  
Atsuo Nomura ◽  
Ryuji Kato ◽  
Masatoshi Miyamura ◽  
...  

2020 ◽  
Vol 11 (10) ◽  
pp. 8547-8559
Author(s):  
Hongjing Zhao ◽  
Yu Wang ◽  
Mengyao Mu ◽  
Menghao Guo ◽  
Hongxian Yu ◽  
...  

Antibiotics are used worldwide to treat diseases in humans and other animals; most of them and their secondary metabolites are discharged into the aquatic environment, posing a serious threat to human health.


2019 ◽  
Vol 476 (24) ◽  
pp. 3705-3719 ◽  
Author(s):  
Avani Vyas ◽  
Umamaheswar Duvvuri ◽  
Kirill Kiselyov

Platinum-containing drugs such as cisplatin and carboplatin are routinely used for the treatment of many solid tumors including squamous cell carcinoma of the head and neck (SCCHN). However, SCCHN resistance to platinum compounds is well documented. The resistance to platinum has been linked to the activity of divalent transporter ATP7B, which pumps platinum from the cytoplasm into lysosomes, decreasing its concentration in the cytoplasm. Several cancer models show increased expression of ATP7B; however, the reason for such an increase is not known. Here we show a strong positive correlation between mRNA levels of TMEM16A and ATP7B in human SCCHN tumors. TMEM16A overexpression and depletion in SCCHN cell lines caused parallel changes in the ATP7B mRNA levels. The ATP7B increase in TMEM16A-overexpressing cells was reversed by suppression of NADPH oxidase 2 (NOX2), by the antioxidant N-Acetyl-Cysteine (NAC) and by copper chelation using cuprizone and bathocuproine sulphonate (BCS). Pretreatment with either chelator significantly increased cisplatin's sensitivity, particularly in the context of TMEM16A overexpression. We propose that increased oxidative stress in TMEM16A-overexpressing cells liberates the chelated copper in the cytoplasm, leading to the transcriptional activation of ATP7B expression. This, in turn, decreases the efficacy of platinum compounds by promoting their vesicular sequestration. We think that such a new explanation of the mechanism of SCCHN tumors’ platinum resistance identifies novel approach to treating these tumors.


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