Role of heme oxygenases in sepsis-induced diaphragmatic contractile dysfunction and oxidative stress

2002 ◽  
Vol 283 (2) ◽  
pp. L476-L484 ◽  
Author(s):  
Esther Barreiro ◽  
Alain S. Comtois ◽  
Shawn Mohammed ◽  
Larry C. Lands ◽  
Sabah N. A. Hussain
Keyword(s):  
Oxidative Stress ◽  
Muscle Protein ◽  
Contractile Dysfunction ◽  
Heme Oxygenases ◽  
Oxide Synthase ◽  
And Oxidative Stress ◽  
Ventilatory Muscles ◽  
Inducible Nitric Oxide

Heme oxygenases (HOs), essential enzymes for heme metabolism, play an important role in the defense against oxidative stress. In this study, we evaluated the expression and functional significance of HO-1 and HO-2 in the ventilatory muscles of normal rats and rats injected with bacterial lipopolysaccharide (LPS). Both HO-1 and HO-2 proteins were detected inside ventilatory and limb muscle fibers of normal rats. Diaphragmatic HO-1 and HO-2 expressions rose significantly within 1 and 12 h of LPS injection, respectively. Inhibition of the activity of inducible nitric oxide synthase (iNOS) in rats and absence of this isoform in iNOS−/− mice did alter sepsis-induced regulation of muscle HOs. Systemic inhibition of HO activity with chromium mesoporphyrin IX enhanced muscle protein oxidation and hydroxynonenal formation in both normal and septic rats. Moreover, in vitro diaphragmatic force generation declined substantially in response to HO inhibition both in normal and septic rats. We conclude that both HO-1 and HO-2 proteins play an important role in the regulation of muscle contractility and in the defense against sepsis-induced oxidative stress.

scholarly journals Aminoguanidine Protects Boar Spermatozoa against the Deleterious Effects of Oxidative Stress

Pharmaceutics ◽  
2018 ◽  
Vol 10 (4) ◽  
pp. 212 ◽  
Author(s):  
Eliana Pintus ◽  
Martin Kadlec ◽  
Marija Jovičić ◽  
Markéta Sedmíková ◽  
José Ros-Santaella
Keyword(s):  
Oxidative Stress ◽  
Therapeutic Agent ◽  
Antioxidant Properties ◽  
In Vitro Effects ◽  
Oxide Synthase ◽  
Boar Spermatozoa ◽  
Generating System ◽  
Control Samples ◽  
Inducible Nitric Oxide

Aminoguanidine is a selective inhibitor of the inducible nitric oxide synthase (iNOS) and a scavenger of reactive oxygen species (ROS). Numerous studies have shown the antioxidant properties of aminoguanidine in several cell lines, but the in vitro effects of this compound on spermatozoa under oxidative stress are unknown. In this study, we tested the hypothesis that aminoguanidine may protect against the detrimental effects of oxidative stress in boar spermatozoa. For this purpose, sperm samples were incubated with a ROS generating system (Fe2+/ascorbate) with or without aminoguanidine supplementation (10, 1, and 0.1 mM). Our results show that aminoguanidine has powerful antioxidant capacity and protects boar spermatozoa against the deleterious effects of oxidative stress. After 2 h and 3.5 h of sperm incubation, the samples treated with aminoguanidine showed a significant increase in sperm velocity, plasma membrane and acrosome integrity together with a reduced lipid peroxidation in comparison with control samples (p < 0.001). Interestingly, except for the levels of malondialdehyde, the samples treated with 1 mM aminoguanidine did not differ or showed better performance than control samples without Fe2+/ascorbate. The results from this study provide new insights into the application of aminoguanidine as an in vitro therapeutic agent against the detrimental effects of oxidative stress in semen samples.

scholarly journals The Role of HO-1 and Its Crosstalk with Oxidative Stress in Cancer Cell Survival

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2401
Author(s):  
Shih-Kai Chiang ◽  
Shuen-Ei Chen ◽  
Ling-Chu Chang
Keyword(s):  
Oxidative Stress ◽  
Redox Regulation ◽  
Oxidative Status ◽  
Multiple Roles ◽  
Mitochondrial Enzymes ◽  
Heme Oxygenases ◽  
Downstream Effects ◽  
Cancer Cell Survival ◽  
And Oxidative Stress

Heme oxygenases (HOs) act on heme degradation to produce carbon monoxide (CO), free iron, ferritin, and biliverdin. Upregulation of cellular HO-1 levels is signature of oxidative stress for its downstream effects particularly under pro-oxidative status. Subcellular traffics of HO-1 to different organelles constitute a network of interactions compromising a variety of effectors such as pro-oxidants, ROS, mitochondrial enzymes, and nucleic transcription factors. Some of the compartmentalized HO-1 have been demonstrated as functioning in the progression of cancer. Emerging data show the multiple roles of HO-1 in tumorigenesis from pathogenesis to the progression to malignancy, metastasis, and even resistance to therapy. However, the role of HO-1 in tumorigenesis has not been systematically addressed. This review describes the crosstalk between HO-1 and oxidative stress, and following redox regulation in the tumorigenesis. HO-1-regulated signaling pathways are also summarized. This review aims to integrate basic information and current progress of HO-1 in cancer research in order to enhance the understandings and facilitate following studies.

SAHA attenuates rotenone-induced toxicity in primary microglia and HT-22 cells

2020 ◽  
pp. 074823372097927
Author(s):  
Caner Günaydin ◽  
Z Betül Çelik ◽  
S Sırrı Bilge ◽  
Bahattin Avci ◽  
Nurten Kara
Keyword(s):  
Oxidative Stress ◽  
Histone Acetylation ◽  
Environmental Chemicals ◽  
Histone Deacetylation ◽  
Epigenetic Alterations ◽  
Primary Mouse ◽  
Factor Α ◽  
Oxide Synthase ◽  
And Oxidative Stress

Rotenone is an industrial and environmental toxicant that has been strongly associated with neurodegeneration. It is clear that rotenone induces inflammatory and oxidative stress; however, information on the role of histone acetylation in neurotoxicity is limited. Epigenetic alterations, neuroinflammation, and oxidative stress play a role in the progression of neurodegeneration and can be caused by exposure to environmental chemicals, such as rotenone. Histone modifications, such as methylation and acetylation, play an important role in mediating epigenetic changes. Therefore, we here investigated the effects of histone acetylation on rotenone-induced inflammation and oxidative stress in both primary mouse microglia and hippocampal HT-22 cells using the pan-histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA). Our results showed that SAHA suppressed the inflammatory response by decreasing nuclear factor kappa B and inducible nitric oxide synthase expression. Additionally, SAHA inhibited the rotenone-induced elevation of interleukin 6 and tumor necrosis factor α levels in both cell lines. Furthermore, SAHA improved the rotenone-induced antioxidant status by mitigating the decrease in cellular glutathione levels. Additionally, SAHA prevented the rotenone-induced increase in the HDAC activity in microglial and hippocampal HT-22 cells. Together, our results showed that SAHA reduced rotenone-induced inflammatory and oxidative stress, suggesting a role for histone deacetylation in environmental-related neurotoxicity.

scholarly journals iNOS Promotes the Development of Osteosarcoma via Wnt/β-Catenin Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Wei Chu ◽  
Lirong Cao ◽  
Gui Daokun ◽  
Jiali Zhao
Keyword(s):  
Tumor Formation ◽  
Inos Expression ◽  
Migration And Invasion ◽  
Potential Therapeutic Target ◽  
Normal Tissues ◽  
Oxide Synthase ◽  
Inos Inhibition ◽  
Inducible Nitric Oxide

Inducible nitric oxide synthase (iNOS), accompanied with protumor and antitumor activity, has been studied in multiple cancers. However, the role of iNOS expression in osteosarcoma (OS) is far from being fully understood. In present work, iNOS levels were detected in OS tissues and cell lines. Colony formation assay, Transwell assay, and fow cytometer were used to assess proliferation, migration, invasion, and apoptosis abilities in vitro after iNOS inhibition. Western blotting determined the expressions of iNOS, MMP2, MMP9, C-MYC, Ki67, PCNA, and β-catenin. Mice transfected with OS cells were to evaluate tumor formation. IHC assay was to evaluate the expressions of iNOS and β-catenin in mice. The results showed that iNOS was upregulated in both OS tissues and cells compared with that in matched normal tissues or cells. And we found that proliferation, migration, and invasion numbers of OS cells were decreased, and apoptosis numbers of OS cells were increased after iNOS inhibition. MMP2, MMP9, C-MYC, Ki67, and PCNA levels were also reduced in OS cells treated with iNOS inhibition. Else, iNOS inhibition would suppress β-catenin expression in OS cells to regulate MMP2, MMP9, C-MYC, Ki67, and PCNA expressions. In addition, tumor formation, iNOS expression, and β-catenin expression were inhibited in mice transplanted with iNOS knockout OS cells. These results indicated that iNOS might be a potential therapeutic target for OS.

scholarly journals Berries and oxidative stress markers: an overview of human intervention studies

2015 ◽  
Vol 6 (9) ◽  
pp. 2890-2917 ◽  
Author(s):  
Cristian Del Bo’ ◽  
Daniela Martini ◽  
Marisa Porrini ◽  
Dorothy Klimis-Zacas ◽  
Patrizia Riso
Keyword(s):  
Oxidative Stress ◽  
Intervention Studies ◽  
Human Intervention ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Intervention Trials ◽  
And Oxidative Stress

Severalin vitroandin vivostudies have demonstrated that polyphenol-rich berries may counteract oxidative stress. In this review, we summarized the main finding from human intervention trials on the role of berries in the modulation of markers of oxidative lipid, protein and DNA damage.

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