Oxidative stress-induced skeletal muscle injury involves in NF-κB/p53-activated immunosuppression and apoptosis response in copper (II) or/and arsenite-exposed chicken

Zhao, Hongjing; Wang, Yu; Shao, Yizhi; Liu, Juanjuan; Wang, Sirui; Xing, Mingwei

doi:10.1016/j.chemosphere.2018.06.165

Cited by 115 publications

(20 citation statements)

References 44 publications

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“…According to the previous studies, exposure of toxicants resulted in the damage of cell and the activation of cell apoptosis, 44‐46 which is consistent with our results that long term radon exposure caused the lung tracheal/bronchial epithelial cells damage and apoptosis in time‐ and dose‐ dependent manners as shown in Figures 2 and 3. Furthermore, we also showed that radon exposure caused mitochondrial dysfunction as indicated by the levels of mtDNA, MMP and ATP, which are related to cell apoptosis.…”

Section: Discussionsupporting

confidence: 92%

“…Moreover, we explored the effect of melatonin on radon caused lung injury and clarified its protective effect as well. (a) We found that radon exposure caused pronounced lung injury in dose-and time-dependent manners, which was character- According to the previous studies, exposure of toxicants resulted in the damage of cell and the activation of cell apoptosis, [44][45][46] which is consistent with our results that long term radon exposure caused the lung tracheal/bronchial epithelial cells damage and apoptosis in timeand dose-dependent manners as shown in Figures 2 and 3. Furthermore, we also showed that radon exposure caused mitochondrial dysfunction as indicated by the levels of mtDNA, MMP and ATP, which are related to cell apoptosis.…”

Section: Discussionsupporting

confidence: 91%

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Protection of melatonin against long‐term radon exposure‐caused lung injury

Fang

Yang

et al. 2020

Environmental Toxicology

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Radon is one of the major pathogenic factors worldwide. Recently, epidemiological studies have suggested that radon exposure plays an important role in lung injury, which could further cause cancer. However, the toxic effects and underlying mechanism on lung injury are still not clear. Here, we identified the detailed toxic effects of long‐term radon exposure. Specifically, the manifestations were inflammatory response and cell apoptosis in dose‐ and time‐dependent manners. In detail, it caused the mitochondrial dysfunction and oxidative stress as determined by the abnormal levels of mitochondrial DNA copy number, adenosine triphosphate, mitochondrial membrane potential, superoxide dismutase, and cycloxygenase‐2. Furthermore, we found that melatonin treatment ameliorated mitochondrial dysfunction and attenuated the levels of oxidative stress caused by long‐term radon exposure, which could further inhibit the lung tissue apoptosis as determined by the decreased levels of cleaved caspase 3. Our study would provide potential therapeutic application of melatonin on lung tissue injury caused by long‐term radon exposure.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionsupporting

confidence: 91%

Protection of melatonin against long‐term radon exposure‐caused lung injury

Fang

Yang

et al. 2020

Environmental Toxicology

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“…Similarly, previous studies have demonstrated increase in P53, iNOS, and CYP1A1 mRNA expression levels with Pb exposure in different cell lines (Song et al 2001;Korashy and El-Kadi 2008;Tousson et al 2011;Al Bakheet et al 2013). These results suggest a possible role for NF-jB and AhR in Pb-triggered immune responses (Yoshizawa et al 2005;Wang et al 2018;Zhao et al 2006Zhao et al , 2018. This conclusion is supported by the observations that AhR and NF-jB signaling pathways mediate lung toxicities (Zhao et al 2006;Yu et al 2013).…”

Section: Control (B)supporting

confidence: 69%

The role of NF-κB and AhR transcription factors in lead-induced lung toxicity in human lung cancer A549 cells

Attafi

Bakheet

Korashy

2019

Toxicology Mechanisms and Methods

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Lead (Pb) is recognized as the first heavy metal of the top six toxic air pollutants threatening human health and the second hazardous substance. Pb exposure is associated with lung impairment and high incidences of lung cancer. Nuclear factor kappa B (NF-jB) and aryl hydrocarbon receptor (AhR) signaling pathways are known to be expressed and play an important role in the lung. However, the link between Pb lung toxicity and NF-jB and/or AhR pathways remains unclear. This study was established to explore the role of NF-jB and AhR modulation in Pb-induced lung toxicity in human lung cancer A549 cells. In the current study, treatment of A549 cells with Pb significantly induced cell apoptosis as evidenced by increasing a) the percentage of cells underwent apoptosis determined by flow cytometry and b) p53 mRNA level. Pb treatment induced oxidative stress by a) increasing the formation of reactive oxygen species and b) decreasing GSTA1 mRNA levels. The toxic effects of Pb on the lung was associated with significant increases in NF-jB and AhR levels which was accompanied with increases in downstream targets genes, iNOS and CYP1A1, respectively. Inhibition of NF-jB or AhR either chemically using resveratrol or genetically using small interfering RNA (siRNA) significantly rescued A549 cells from Pb-mediated lung toxicity. The results clearly indicate that Pb-mediated lung toxicities are NF-jB and AhR-dependent mechanism.

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“…Environmental challenge exposure, such as cadmium, arsenic, and lead, could induce oxidative stress through elevating ROS and MDA levels, decreasing the activities of glutathione peroxidase (GPX) and SOD [37–39]. Besides, environmental gases, such as PM2.5, cigarette smoke, NH 3 , SO 2 , nitrogen dioxide (NO 2 ), and ozone (O 3 ), could lead to oxidative stress, and the mitochondria were also damaged by varying degrees, in more detail, of changes manifested as the increased levels of MDA and the decreased levels of total superoxide dismutase (T-SOD) [40–45].…”

Section: Discussionmentioning

confidence: 99%

Hydrogen Sulfide Gas Exposure Induces Necroptosis and Promotes Inflammation through the MAPK/NF-κB Pathway in Broiler Spleen

Chi

Wang

2019

Oxidative Medicine and Cellular Longevity

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Hydrogen sulfide (H2S) is one of the main pollutants in the atmosphere, which is a serious threat to human health. The decomposition of sulfur-containing organics in chicken houses could produce a large amount of H2S, thereby damaging poultry health. In this study, one-day-old broilers were selected and exposed to 4 or 20 ppm of H2S gas (0-3 weeks: 4±0.5 ppm, 4-6 weeks: 20±0.5 ppm). The spleen samples were collected immediately after the chickens were euthanized at 2, 4, and 6 weeks. The histopathological and ultrastructural observations showed obvious necrosis characteristics of H2S-exposed spleens. H2S exposure suppressed GSH, CAT, T-AOC, and SOD activities; increased NO, H2O2, and MDA content and iNOS activity; and induced oxidative stress. ATPase activities and the expressions of energy metabolism-related genes were significantly decreased. Also, the expressions of related necroptosis (RIPK1, RIPK3, MLKL, TAK1, TAB2, and TAB3) were significantly increased, and the MAPK pathway was activated. Besides, H2S exposure activated the NF-κB classical pathway and induced TNF-α and IL-1β release. Taken together, we conclude that H2S exposure induces oxidative stress and energy metabolism dysfunction; evokes necroptosis; activates the MAPK pathway, eventually triggering the NF-κB pathway; and promotes inflammatory response in chicken spleens.

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Oxidative stress-induced skeletal muscle injury involves in NF-κB/p53-activated immunosuppression and apoptosis response in copper (II) or/and arsenite-exposed chicken

Cited by 115 publications

References 44 publications

Protection of melatonin against long‐term radon exposure‐caused lung injury

Protection of melatonin against long‐term radon exposure‐caused lung injury

The role of NF-κB and AhR transcription factors in lead-induced lung toxicity in human lung cancer A549 cells

Hydrogen Sulfide Gas Exposure Induces Necroptosis and Promotes Inflammation through the MAPK/NF-κB Pathway in Broiler Spleen

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