Effects of CEES and LPS synergistically stimulate oxidative stress inactivates OGG1 signaling in macrophage cells

Sagar, Satish; Kumar, Pranaw; Behera, Reena Rani; Pal, Arttatrana

doi:10.1016/j.jhazmat.2014.05.096

Cited by 21 publications

(22 citation statements)

References 42 publications

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“…A number of studies showed that lipopolysaccharide could induce excessive ROS generation and apoptosis events in different cell lines [22, 23, 38, 39]. As expected, we found that lipopolysaccharide treatment significantly increased intracellular ROS levels and the early apoptotic rate in bovine oocytes.…”

Section: Discussionsupporting

confidence: 88%

“…Oxidative stress can negatively affect spindle integrity and biological function [20], lower meiotic resumption rates [21], and then decrease oocyte maturation potential. Numerous studies have shown that lipopolysaccharide could induce cytotoxicity by enhancing cellular oxidative stress in different cell lines, including macrophage cell [22], dendritic cell [23], and epithelial cell [24]. The intracellular glutathione-dependent redox homeostasis could be altered by lipopolysaccharide exposure [22].…”

Section: Introductionmentioning

confidence: 99%

“…Numerous studies have shown that lipopolysaccharide could induce cytotoxicity by enhancing cellular oxidative stress in different cell lines, including macrophage cell [22], dendritic cell [23], and epithelial cell [24]. The intracellular glutathione-dependent redox homeostasis could be altered by lipopolysaccharide exposure [22]. Moreover, Raza et al reported that lipopolysaccharide could induces apoptosis by increasing the expression of oxidative stress-sensitive genes and proteins, and releasing the pro-apoptotic factor mitochondrial cytochrome c from the mitochondrial intermembrane space into the cytoplasm [25].…”

Section: Introductionmentioning

confidence: 99%

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Effects of lipopolysaccharide on maturation of bovine oocyte in vitro and its possible mechanisms

et al. 2016

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Lipopolysaccharide disturbs the secretion of gonadotropin, endometrial function and implantation efficiency. However, there is little information regarding the effects of lipopolysaccharide on cyclic ovary activity, especially oocyte maturation. Therefore, we aimed to investigate the effects of lipopolysaccharide on the maturation potential of bovine oocytes. We found that lipopolysaccharide exposure significantly decreased the first polar body extrusion rate and delayed the cell cycle progression. The abnormal spindle rate was significantly increased in lipopolysaccharide treatment group, accompanied by disrupted localization and level of phosphorylated mitogen-activated protein kinase (p-MAPK). Moreover, lipopolysaccharide treatment significantly increased intracellular reactive oxygen species (ROS) levels and the early apoptotic rate in oocytes. The pro-apoptotic caspase-3 and Bax mRNA levels and caspase-3 protein level were significantly increased, whereas the anti-apoptotic Bcl-2 and XIAP transcript abundance were significantly decreased in lipopolysaccharide exposure group. Furthermore, the dimethyl-histone H3 lysine 4 (H3K4me2) level was significantly increased, while the DNA methylation (5-mC) and dimethyl-histone H3 lysine 9 (H3K9me2) levels were markedly decreased in oocytes treated with lipopolysaccharide. In conclusion, lipopolysaccharide exposure inhibits the maturation potential of bovine oocytes by affecting cell cycle, cytoskeletal dynamics, oxidative stress, and epigenetic modifications.

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Section: Discussionsupporting

confidence: 88%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effects of lipopolysaccharide on maturation of bovine oocyte in vitro and its possible mechanisms

et al. 2016

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“…These beneficial effects of NAC are likely related to its antioxidant and anti-inflammatory activity. In cultured macrophages, NAC inhibits the generation of reactive oxygen and nitrogen species induced by CEES and upregulates antioxidants (Sagar et al, 2014). It may also facilitate tissue growth and repair following SM exposure by improving vascularization (Steinritz et al, 2010).…”

Section: Targeting Reactive Oxygen and Nitrogen Speciesmentioning

confidence: 99%

Mustard vesicant-induced lung injury: Advances in therapy

Weinberger

Malaviya

Sunil

et al. 2016

Toxicology and Applied Pharmacology

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Most mortality and morbidity following exposure to vesicants such as sulfur mustard is due to pulmonary toxicity. Acute injury is characterized by epithelial detachment and necrosis in the pharynx, trachea and bronchioles, while long-term consequences include fibrosis and in some instances, cancer. Current therapies to treat mustard poisoning are primarily palliative and do not target underlying pathophysiologic mechanisms. New knowledge about vesicant-induced pulmonary disease pathogenesis has led to the identification of potentially efficacious strategies to reduce injury by targeting inflammatory cells and mediators including reactive oxygen and nitrogen species, proteases and proinflammatory/cytotoxic cytokines. Therapeutics under investigation include corticosteroids, N-acetyl cysteine, which has both mucolytic and antioxidant properties, inducible nitric oxide synthase inhibitors, liposomes containing superoxide dismutase, catalase, and/or tocopherols, protease inhibitors, and cytokine antagonists such as anti-tumor necrosis factor (TNF)-α antibody and pentoxifylline. Antifibrotic and fibrinolytic treatments may also prove beneficial in ameliorating airway obstruction and lung remodeling. More speculative approaches include inhibitors of transient receptor potential channels, which regulate pulmonary epithelial cell membrane permeability, non-coding RNAs and mesenchymal stem cells. As mustards represent high priority chemical threat agents, identification of effective therapeutics for mitigating toxicity is highly significant.

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“…Despite these reports, surprisingly little is known about the mechanism how LPS causes G0 arrest. It has been suggested that production of ROS or DNA damage can play role 34, 35 . Our data suggest that neither ROS nor DNA damage seems to be responsible for G0 arrest in human MDM (Fig.S2, S3).…”

Section: Discussionmentioning

confidence: 99%

IFN-independent G0 arrest and SAMHD1 activation following TLR4 activation in macrophages

Mlčochová

Winstone²,

Zuliani-Alvarez³

et al. 2019

Preprint

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Effects of CEES and LPS synergistically stimulate oxidative stress inactivates OGG1 signaling in macrophage cells

Cited by 21 publications

References 42 publications

Effects of lipopolysaccharide on maturation of bovine oocyte in vitro and its possible mechanisms

Effects of lipopolysaccharide on maturation of bovine oocyte in vitro and its possible mechanisms

Mustard vesicant-induced lung injury: Advances in therapy

IFN-independent G0 arrest and SAMHD1 activation following TLR4 activation in macrophages

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