Non-enzymatic antioxidant responses of Mytilus galloprovincialis: Insights into the physiological role against metal-induced oxidative stress

2021 ◽  
Vol 240 ◽  
pp. 108909 ◽  
Author(s):  
Gianfranco Santovito ◽  
Erika Trentin ◽  
Ilaria Gobbi ◽  
Paola Bisaccia ◽  
Laura Tallandini ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mytilus Galloprovincialis ◽  
Physiological Role ◽  
Antioxidant Responses ◽  
Enzymatic Antioxidant

scholarly journals Non-Enzymatic Antioxidant Responses of Mytilus galloprovincialis under Cadmium-Induced Oxidative Stress Risk

2020 ◽  
Author(s):  
Gianfranco Santovito ◽  
Erika Trentin ◽  
Ilaria Gobbi ◽  
Paola Bisaccia ◽  
Laura Tallandini ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mytilus Galloprovincialis ◽  
Model Organism ◽  
Antioxidant Defenses ◽  
Marine Bivalve ◽  
Metal Sequestration ◽  
Enzymatic Antioxidant ◽  
Blue Mussels ◽  
Living Organisms ◽  
Cellular Components

Exposure to metals is known to generate oxidative stress in living organisms, which are able to respond with the induction of antioxidant defenses, both enzymatic and non-enzymatic. The aim of this work is to study the correlation among several non-enzymatic component of the antioxidant system, that are physiologically related to both metal sequestration and defense against metal-induced oxidative stress, using the blue mussels (Mytilus galloprovincialis) as model organism. Specimens of this marine bivalve were experimentally exposed to cadmium (Cd), used as oxidative stress risk inducer. Cd, metallothionein (MT), glutathione (GSH), malondialdehyde (MDA) contents, and glutathione reductase (GR) activity in gills and in digestive glands were assessed at 0, 12, 24, 48, 72 and 96 h. The obtained results provide new data about the relationships among the non-enzymatic antioxidant cellular components considered in this study. These constitute the prompt physiological responses to the risk of oxidative stress in blue mussels exposed to Cd in controlled laboratory conditions.

scholarly journals The Phosphoarginine Phosphatase PtpB from Staphylococcus aureus Is Involved in Bacterial Stress Adaptation during Infection

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 645
Author(s):  
Mohamed Ibrahem Elhawy ◽  
Sylvaine Huc-Brandt ◽  
Linda Pätzold ◽  
Laila Gannoun-Zaki ◽  
Ahmed Mohamed Mostafa Abdrabou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Staphylococcus Aureus ◽  
Treatment Strategies ◽  
Physiological Role ◽  
Aureus Strain ◽  
Stress Adaptation ◽  
Cellular Mechanisms ◽  
Host Interaction ◽  
Liver And Kidney

Staphylococcus aureus continues to be a public health threat, especially in hospital settings. Studies aimed at deciphering the molecular and cellular mechanisms that underlie pathogenesis, host adaptation, and virulence are required to develop effective treatment strategies. Numerous host-pathogen interactions were found to be dependent on phosphatases-mediated regulation. This study focused on the analysis of the role of the low-molecular weight phosphatase PtpB, in particular, during infection. Deletion of ptpB in S. aureus strain SA564 significantly reduced the capacity of the mutant to withstand intracellular killing by THP-1 macrophages. When injected into normoglycemic C57BL/6 mice, the SA564 ΔptpB mutant displayed markedly reduced bacterial loads in liver and kidney tissues in a murine S. aureus abscess model when compared to the wild type. We also observed that PtpB phosphatase-activity was sensitive to oxidative stress. Our quantitative transcript analyses revealed that PtpB affects the transcription of various genes involved in oxidative stress adaptation and infectivity. Thus, this study disclosed first insights into the physiological role of PtpB during host interaction allowing us to link phosphatase-dependent regulation to oxidative bacterial stress adaptation during infection.

B- to Plasma-Cell Terminal Differentiation Entails Oxidative Stress and Profound Reshaping of the Antioxidant Responses

2010 ◽  
Vol 13 (8) ◽  
pp. 1133-1144 ◽  
Author(s):  
Milena Bertolotti ◽  
Sun Hee Yim ◽  
Jose M. Garcia-Manteiga ◽  
Silvia Masciarelli ◽  
Yoo-Jin Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Plasma Cell ◽  
Terminal Differentiation ◽  
Antioxidant Responses

scholarly journals N-acetyl-cysteine increases cellular dysfunction in progressive chronic kidney damage after acute kidney injury by dampening endogenous antioxidant responses

2018 ◽  
Vol 314 (5) ◽  
pp. F956-F968 ◽  
Author(s):  
David M. Small ◽  
Washington Y. Sanchez ◽  
Sandrine F. Roy ◽  
Christudas Morais ◽  
Heddwen L. Brooks ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Mitochondrial Dysfunction ◽  
Transforming Growth Factor ◽  
Multiphoton Microscopy ◽  
Kidney Injury ◽  
Peroxisome Proliferator ◽  
Fluorescence Lifetime Imaging ◽  
Antioxidant Responses ◽  
Acetyl Cysteine

Oxidative stress and mitochondrial dysfunction exacerbate acute kidney injury (AKI), but their role in any associated progress to chronic kidney disease (CKD) remains unclear. Antioxidant therapies often benefit AKI, but their benefits in CKD are controversial since clinical and preclinical investigations often conflict. Here we examined the influence of the antioxidant N-acetyl-cysteine (NAC) on oxidative stress and mitochondrial function during AKI (20-min bilateral renal ischemia plus reperfusion/IR) and progression to chronic kidney pathologies in mice. NAC (5% in diet) was given to mice 7 days prior and up to 21 days post-IR (21d-IR). NAC treatment resulted in the following: prevented proximal tubular epithelial cell apoptosis at early IR (40-min postischemia), yet enhanced interstitial cell proliferation at 21d-IR; increased transforming growth factor-β1 expression independent of IR time; and significantly dampened nuclear factor-like 2-initiated cytoprotective signaling at early IR. In the long term, NAC enhanced cellular metabolic impairment demonstrated by increased peroxisome proliferator activator-γ serine-112 phosphorylation at 21d-IR. Intravital multiphoton microscopy revealed increased endogenous fluorescence of nicotinamide adenine dinucleotide (NADH) in cortical tubular epithelial cells during ischemia, and at 21d-IR that was not attenuated with NAC. Fluorescence lifetime imaging microscopy demonstrated persistent metabolic impairment by increased free/bound NADH in the cortex at 21d-IR that was enhanced by NAC. Increased mitochondrial dysfunction in remnant tubular cells was demonstrated at 21d-IR by tetramethylrhodamine methyl ester fluorimetry. In summary, NAC enhanced progression to CKD following AKI not only by dampening endogenous cellular antioxidant responses at time of injury but also by enhancing persistent kidney mitochondrial and metabolic dysfunction.

Salt tolerance of the halophyte Limonium delicatulum is more associated with antioxidant enzyme activities than phenolic compounds

2016 ◽  
Vol 43 (7) ◽  
pp. 607 ◽  
Author(s):  
Souid Aymen ◽  
Gabriele Morena ◽  
Longo Vincenzo ◽  
Pucci Laura ◽  
Bellani Lorenza ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Photosynthetic Performance ◽  
Polyphenolic Compounds ◽  
Antioxidant Enzyme Activities ◽  
Strongly Correlated ◽  
Growth Responses ◽  
Antioxidant Responses ◽  
Stress Markers ◽  
Biochemical Assays ◽  
Nacl Concentration

In this work we studied the effect of salinity (ranging from 50 to 500 mM NaCl) on the physiological and the antioxidant responses of the local halophyte Limonium delicatulum Kuntze. We based our analysis on 12 biochemical assays that are commonly used to measure the antioxidant responses under stress such as oxidative stress markers, enzymes activities and polyphenolic compounds. Our aim was to study parameters that are strongly correlated with the growth response to salinity. Results showed two different growth responses depending on the concentration of NaCl in the medium. Under 50 to 200 mM, the growth was stimulated before it decreased significantly at 300–500 mM. L. delicatulum revealed a good aptitude to maintain photosynthetic machinery by increasing the concentrations of photosynthetic pigments, which is essential for the stabilisation of photosystems and the photosynthesis process under optimal NaCl concentration. Their breakdown at higher salinity decreased the photosynthetic performance of plants resulting in growth inhibition. Moreover, to reduce the damaging effect of oxidative stress and to tolerate the accumulation of salt ions, L. delicatulum induced the activities of their antioxidant enzymes more than their contents in polyphenolic compounds.

scholarly journals Identification and Molecular Characterization of Superoxide Dismutases Isolated From A Scuticociliate Parasite: Physiological Role in Oxidative Stress

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Iria Folgueira ◽  
Jesús Lamas ◽  
Ana Paula de Felipe ◽  
Rosa Ana Sueiro ◽  
José Manuel Leiro
Keyword(s):  
Oxidative Stress ◽  
Physiological Role ◽  
Host Immune System ◽  
Farmed Fish ◽  
Free Living ◽  
Antioxidant Defences ◽  
Sod Activity ◽  
Cellular Protection ◽  
Facultative Parasite ◽  
Copper Zinc

Abstract Philasterides dicentrarchi is a free-living microaerophilic scuticociliate that can become a facultative parasite and cause a serious parasitic disease in farmed fish. Both the free-living and parasitic forms of this scuticociliate are exposed to oxidative stress associated with environmental factors and the host immune system. The reactive oxygen species (ROS) generated by the host are neutralized by the ciliate by means of antioxidant defences. In this study we aimed to identify metalloenzymes with superoxide dismutase (SOD) activity capable of inactivating the superoxide anion (•O2−) generated during induction of oxidative stress. P. dicentrarchi possesses the three characteristic types of SOD isoenzymes in eukaryotes: copper/zinc-SOD, manganese-SOD and iron-SOD. The Cu/Zn-SOD isoenzymes comprise three types of homodimeric proteins (CSD1-3) of molecular weight (MW) 34–44 kDa and with very different AA sequences. All Cu/Zn-SODs are sensitive to NaCN, located in the cytosol and in the alveolar sacs, and one of them (CSD2) is extracellular. Mn- and Fe-SOD transcripts encode homodimeric proteins (MSD and FSD, respectively) in their native state: a) MSD (MW 50 kDa) is insensitive to H2O2 and NaN3 and is located in the mitochondria; and b) FSD (MW 60 kDa) is sensitive to H2O2, NaN3 and the polyphenol trans-resveratrol and is located extracellularly. Expression of SOD isoenzymes increases when •O2− is induced by ultraviolet (UV) irradiation, and the increase is proportional to the dose of energy applied, indicating that these enzymes are actively involved in cellular protection against oxidative stress.

scholarly journals Role of Mitochondrial Cytochrome P450 2E1 in Healthy and Diseased Liver

Cells ◽  
2022 ◽  
Vol 11 (2) ◽  
pp. 288
Author(s):  
Julie Massart ◽  
Karima Begriche ◽  
Jessica H. Hartman ◽  
Bernard Fromenty
Keyword(s):  
Oxidative Stress ◽  
Cytochrome P450 ◽  
Liver Disease ◽  
Fatty Liver ◽  
Current Knowledge ◽  
Physiological Role ◽  
Experimental Investigations ◽  
Rat Liver Mitochondria ◽  
Cytochrome P450 2E1

Cytochrome P450 2E1 (CYP2E1) is pivotal in hepatotoxicity induced by alcohol abuse and different xenobiotics. In this setting, CYP2E1 generates reactive metabolites inducing oxidative stress, mitochondrial dysfunction and cell death. In addition, this enzyme appears to play a role in the progression of obesity-related fatty liver to nonalcoholic steatohepatitis. Indeed, increased CYP2E1 activity in nonalcoholic fatty liver disease (NAFLD) is deemed to induce reactive oxygen species overproduction, which in turn triggers oxidative stress, necroinflammation and fibrosis. In 1997, Avadhani’s group reported for the first time the presence of CYP2E1 in rat liver mitochondria, and subsequent investigations by other groups confirmed that mitochondrial CYP2E1 (mtCYP2E1) could be found in different experimental models. In this review, we first recall the main features of CYP2E1 including its role in the biotransformation of endogenous and exogenous molecules, the regulation of its expression and activity and its involvement in different liver diseases. Then, we present the current knowledge on the physiological role of mtCYP2E1, its contribution to xenobiotic biotransformation as well as the mechanism and regulation of CYP2E1 targeting to mitochondria. Finally, we discuss experimental investigations suggesting that mtCYP2E1 could have a role in alcohol-associated liver disease, xenobiotic-induced hepatotoxicity and NAFLD.

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