scholarly journals Oxidative stress protein Oxr1 promotes V‐ATPase holoenzyme disassembly in catalytic activity‐independent manner

2021 ◽  
Author(s):  
Md. Murad Khan ◽  
Seowon Lee ◽  
Sergio Couoh‐Cardel ◽  
Rebecca A Oot ◽  
Hyunmin Kim ◽  
...  
2016 ◽  
Vol 33 (2) ◽  
pp. 171-181 ◽  
Author(s):  
Bing Xia ◽  
Kangcheng Chen ◽  
Yingnan Lv ◽  
Damin Huang ◽  
Jing Liu ◽  
...  

Objectives: Methylcyclopentadienyl manganese tricarbonyl (MMT) is an organic derivative of manganese (Mn) and is used as an antiknock agent and octane enhancer in gasoline. In this article, we tested the oxidative stress and heat stress protein (Hsp) 70 levels of gasoline station attendants to explore potential plasma biomarkers. Furthermore, the dose–response relationship was also identified. Methods: A total of 144 workers, including 96 petrol fillers and 48 cashiers, participated in the study. Ambient concentrations of benzene, toluene, ethylbenzene, and xylene (BTEX) and Mn were monitored at nine filling stations. During the measuring process, the individual cumulative exposure index was calculated. Plasma oxidative stress and Hsp70 levels were also analysed using enzyme-linked immunosorbent assay. Results: The BTEX time-weighted average in office areas was significantly lower than in refuelling areas ( p < 0.05). In refuelling areas, the content of Mn ranged from 6.44 μg/m3 to 127.34 μg/m3, which was much higher than that in office areas (3.16–7.22 μg/m3; p < 0.05). Exposed workers had significantly different plasma oxidative stress indicators compared with the control group, respectively: superoxide dismutase (SOD), 39.18 ± 6.05 U/mL versus 52.84 ± 3.87 U/mL; glutathione peroxidase (GSH-Px), 186.07 ± 15.63 U versus 194.38 ± 10.42 U; and malondialdehyde (MDA), 1.68 ± 0.52 nmol/L versus 1.43 ± 0.64 nmol/L (in all comparisons, p < 0.05). Plasma Hsp70 level in the exposed group (2.77 ± 0.64 ng/mL) was significantly higher than in the control group (2.32 ± 0.87 ng/mL; p < 0.05). Furthermore, Hsp70 levels were inversely correlated with the activities of SOD ( r = −0.305) and GSH-Px ( r = −0.302) in the exposed group ( p < 0.05). Moreover, a positive correlation ( r = 0.653) was found between plasma Hsp70 levels and plasma MDA levels ( p < 0.05). Conclusion: Exposure to MMT-containing gasoline may result in increasing reactive oxygen stress among filling station attendants. Plasma Hsp70 levels could be used as a sensitive responsive biomarker for exposed workers.


1995 ◽  
Vol 309 (2) ◽  
pp. 453-459 ◽  
Author(s):  
L Tacchini ◽  
G Pogliaghi ◽  
L Radice ◽  
E Anzon ◽  
A Bernelli-Zazzera

Post-ischaemic reperfusion increases the level of the major heat-shock (stress) protein hsp 70 and of its mRNA by transcriptional mechanisms, and activates the binding of the heat-shock factor HSF to the consensus sequence HSE. In common with CoCl2 treatment, post-ischaemic reperfusion increases the level of haem oxygenase mRNA, an indicator of oxidative stress, but CoCl2 does not seem to induce the expression of the hsp 70 gene [Tacchini, Schiaffonati, Pappalardo, Gatti and Bernelli-Zazzera (1993) Lab. Invest. 68, 465-471]. Starting from these observations, we have now studied the expression of two genes of the hsp 70 family and of other possibly related genes under conditions of oxidative stress. Three different chemicals, which cause oxidative stress by various mechanisms and induce haem oxygenase, enhance the expression of the cognate hsc 73 gene, but do not activate the inducible hsp 70 gene. Expression of the other genes that have been studied seems to vary in intensity and/or time course, in relation to the particular mechanism of action of any single agent. The pattern of induction of the early-immediate response genes c-fos and c-jun observed during oxidative stress differs from that found in post-ischaemic reperfused livers. Oxidative-stress-inducing agents do not promote the binding of HSF to its consensus sequence HSE, such as occurs in heat-shock and post-ischaemic reperfusion, and fail to activate AP-1 (activator protein 1). With the possible exception of Phorone, the oxidative stress chemically induced in rat liver activates NFkB (nuclear factor kB) and AP-2 (activator protein 2) transcription factors.


2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Zonghao Tang ◽  
Jiajie Chen ◽  
Zhenghong Zhang ◽  
Jingjing Bi ◽  
Renfeng Xu ◽  
...  

The increase of oxidative stress is one of the important characteristics of mammalian luteal regression. Previous investigations have revealed the essential role of reactive oxygen species (ROS) in luteal cell death during luteolysis, while it is unknown how ROS is regulated in this process. Considering the decrease of blood flow and increase of PGF2α during luteolysis, we hypothesized that the HIF-1α pathway may be involved in the regulation of ROS in the luteal cell of the late corpus luteum (CL). Here, by using a pseudopregnant rat model, we showed that the level of both HIF-1α and its downstream BNIP3 was increased during luteal regression. Consistently, we observed the increase of autophagy level during luteolysis, which is regulated in a Beclin1-independent manner. Comparing with early (Day 7 of pseudopregnancy) and middle CL (Day 14), the level of ROS was significantly increased in late CL, indicating the contribution of oxidative stress in luteolysis. Inhibition of HIF-1α by echinomycin (Ech), a potent HIF-1α inhibitor, ameliorated the upregulation of BNIP3 and NIX, as well as the induction of autophagy and the accumulation of ROS in luteal cells on Day 21 of pseudopregnancy. Morphologically, Ech treatment delayed the atrophy of the luteal structure at the late-luteal stage. An in vitro study indicated that inhibition of HIF-1α can also attenuate PGF2α-induced ROS and luteal cell apoptosis. Furthermore, the decrease of cell apoptosis can also be observed by ROS inhibition under PGF2α treatment. Taken together, our results indicated that HIF-1α signaling is involved in the regression of CL by modulating ROS production via orchestrating autophagy. Inhibition of HIF-1α could obviously hamper the apoptosis of luteal cells and the process of luteal regression.


2020 ◽  
Author(s):  
Andrew O’Connor ◽  
Rita Berisio ◽  
Mary Lucey ◽  
Kirsten Schaffer ◽  
Siobhán McClean

SummaryUniversal stress proteins (USPs) are ubiquitously expressed in bacteria, plants and eukaryotes and play a lead role in adaptation to environmental conditions. In Gram negative bacteria they enable adaption of bacterial pathogens to the conditions encountered in the human niche, including hypoxia, oxidative stress, osmotic stress, nutrient deficiency or acid stress, thereby facilitating colonisation. We previously reported that all six USP proteins encoded within a low-oxygen responsive locus in Burkholderia cenocepacia showed increased abundance during chronic colonisation of the CF lung. However, the role of USPs in chronic infection is not known. Using mutants derived from B. cenocepacia strain, K56-2, we show that USP76 is required for growth and survival in many conditions associated with the CF lung including, hypoxia, acidic conditions, oxidative stress. Moreover, it is involved in attachment to host epithelial cells, but not virulence. It also has a role in survival in macrophages isolated from people with CF. In contrast, another USP encoded in the same locus, USP92 had no effect on host cell attachment or oxidative stress, but was responsible for a 3-fold increase in virulence. Overall this shows that these USPs, both upregulated during chronic infection, have distinct roles in Burkholderia pathogenesis and may support the survival of B. cenocepacia in the CF lung. Specifically, USP76 is involved in its survival within CF macrophages, a hallmark of Burkholderia infection.


2019 ◽  
Vol 17 (1) ◽  
Author(s):  
P. M. Abruzzo ◽  
A. Matté ◽  
A. Bolotta ◽  
E. Federti ◽  
A. Ghezzo ◽  
...  

Abstract Background It has been established that children with Autism Spectrum Disorders (ASD) are affected by oxidative stress, the origin of which is still under investigation. In the present work, we evaluated inflammatory and pro-oxidant soluble signature in non-syndromic ASD and age-matched typically developing (TD) control children. Methods We analyzed leukocyte gene expression of inflammatory cytokines and inflammation/oxidative-stress related molecules in 21 ASD and 20 TD children. Moreover, in another—comparable—group of non-syndromic ASD (N = 22) and TD (N = 21) children, we analyzed for the first time the protein expression of the four members of the antioxidant enzyme family of peroxiredoxins (Prx) in both erythrocyte membranes and in plasma. Results The gene expression of IL6 and of HSP70i, a stress protein, was increased in ASD children. Moreover, gene expression of many inflammatory cytokines and inflammation/oxidative stress-related proteins correlated with clinical features, and appeared to be linked by a complex network of inter-correlations involving the Aryl Hydrocarbon Receptor signaling pathway. In addition, when the study of inter-correlations within the expression pattern of these molecules was extended to include the healthy subjects, the intrinsic physiological relationships of the inflammatory/oxidative stress network emerged. Plasma levels of Prx2 and Prx5 were remarkably increased in ASD compared to healthy controls, while no significant differences were found in red cell Prx levels. Conclusions Previous findings reported elevated inflammatory cytokines in the plasma of ASD children, without clearly pointing to the presence of neuro-inflammation. On the other hand, the finding of microglia activation in autoptic specimens was clearly suggesting the presence of neuro-inflammation in ASD. Given the role of peroxiredoxins in the protection of brain cells against oxidative stress, the whole of our results, using peripheral data collected in living patients, support the involvement of neuro-inflammation in ASD, and generate a rational for neuro-inflammation as a possible therapeutic target and for plasma Prx5 as a novel indicator of ASD severity.


Biomolecules ◽  
2020 ◽  
Vol 10 (5) ◽  
pp. 809
Author(s):  
Jarmo Laihia ◽  
Kai Kaarniranta

Trehalose is a natural disaccharide synthesized in various life forms, but not found in vertebrates. An increasing body of evidence demonstrates exceptional bioprotective characteristics of trehalose. This review discusses the scientific findings on potential functions of trehalose in oxidative stress, protein clearance, and inflammation, with an emphasis on animal models and clinical trials in ophthalmology. The main objective is to help understand the beneficial effects of trehalose in clinical trials and practice, especially in patients suffering from ocular surface disease. The discussion is supplemented with an overview of patents for the use of trehalose in dry eye and with prospects for the 2020s.


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