ROS-mediated PPAR/RXR inhibition contributes to acetochlor-induced apoptosis and autophagy in Ctenopharyngodon idella hepatic cells

Li, Xiaojing; Bai, Ruichen; Bai, Yichen; Xu, Shiwen; Yang, Yuhong; Xu, Shiwen

doi:10.1016/j.fsi.2022.08.053

Cited by 51 publications

(4 citation statements)

References 60 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The hematoxylin and eosin (H&E) staining method had been described in a previous study. 50 Fresh heart tissues were rapidly fixed in 10% formaldehyde for at least 24 h, washed with running water, dehydrated, transparent, and embedded in paraffin for microscopic examination. 51 The paraffin blocks were cut into sections (5 μm thick) and then stained with H&E for optical microscopic observation.…”

Section: Histopathological Examination Of the Heart Tissuesmentioning

confidence: 99%

Decreased thioredoxin reductase 3 expression promotes nickel‐induced damage to cardiac tissue via activating oxidative stress‐induced apoptosis and inflammation

Liu

et al. 2022

Environmental Toxicology

View full text Add to dashboard Cite

Thioredoxin reductase 3 (Txnrd3) plays a crucial role in antioxidant and anti-cancer activities, and sperm maturation. The damage of heavy metals, including Nickel (Ni), is the most prominent harm in social development, and hampering Txnrd3 might exacerbate Ni-induced cardiac damage. In this study, a total of 160 8-week-old C57BL/N male mice with 25-30 g weight of Txnrd3+/+ wild-type and Txnrd3À/À homozygote-type were randomly divided into eight groups. The mice in the control and Ni groups were gavaged with distilled water and a freshly prepared 10 mg/kg NiCl 2 solution. Melatonin (Mel) groups were administered at a concentration of 2 mg/kg for 21 days at the mice's 0.1 ml/10 g body weight. Ni exposure up-regulated the messenger RNA (mRNA) levels of mitochondrial apoptosis (caspase-3, caspase-9, cytochrome c, p53, and BAX), autophagy (LC3, ATG 1, ATG 7, and Beclin-1), and inflammation (TNF-α, COX 2, IL-1β, IL-2, IL-6, and IL-7)-related markers, but downregulated the mRNA levels of BCL-2, p62 and mTOR (p < .05). Ni exposure decreased the expression of BCL-2 and p62 protein but increased the expression levels of caspase-3, caspase-9, cytochrome c, p53, BAX, ATG 7, Beclin-1, TNF-α, COX 2, IL-1β and IL-2 protein (p < .05). Ni increased the contents of glutathione disulfide (GSSG) and malondialdehyde (MDA) and decreased the activities of catalase (CAT) and total superoxide dismutase (T-SOD) (p < .05). Decreased Txnrd3 expression significantly exacerbated changes compared to the Ni exposure (p < .05). Mel significantly attenuated these changes, but the effect decreased when Txnrd3 was inhibited (p < .05). In conclusion, decreased Txnrd3 expression promoted Ni-induced mitochondrial apoptosis and inflammation via oxidative stress and aggravated heart damage in mice. Decreased Txnrd3 expression significantly reduced the protective effect of Mel to Ni exposure.

show abstract

Section: Histopathological Examination Of the Heart Tissuesmentioning

confidence: 99%

Decreased thioredoxin reductase 3 expression promotes nickel‐induced damage to cardiac tissue via activating oxidative stress‐induced apoptosis and inflammation

Liu

et al. 2022

Environmental Toxicology

View full text Add to dashboard Cite

show abstract

“…The CIK cells of the Con group were cultured with 10% medium. CIK cells in the L‐MPs group were treated with L‐MPs (0.012 mg L −1 ), and the M‐MPs group (0.0625 mg L −1 ), and H‐MPs (0.5 mg L −1 ) + NAC (1 mM) 25 for 24 h.…”

Section: Methodsmentioning

confidence: 99%

Polystyrene microplastics mediate cell cycle arrest, apoptosis, and autophagy in the G2/M phase through ROS in grass carp kidney cells

Lu,

Hou,

Zhang

et al. 2023

Environmental Toxicology

View full text Add to dashboard Cite

Microplastics (MPs) have attracted widespread worldwide attention as a new pollutant. However, the role of reactive oxygen species (ROS) and cell cycle in nephrotoxicity induced by different concentrations of polystyrene microplastics (PS‐MPs) is unknown. This study used grass carp kidney cells (CIK) treated with different concentrations of PS‐MPs (0, 0.012, 0.0625, and 0.5 mg L−1) as subjects. With the increase of PS‐MPs concentration, the levels of ROS and malonaldehyde increased, while the level of total antioxidant capacity, superoxide Dismutase (SOD), and glutathione (GSH) activity decreased. The expression of BUB1 mitotic checkpoint serine/threonine kinase (BUB1), cyclin‐dependent kinase (CDK1), CDK2, CyclinB1, cell division cycle 20 homolog (CDC20), and B‐cell lymphoma‐2, sequestosome 1 decreased significantly. Nevertheless, the expression of Caspase 3, Cleave‐Caspase 3, cytochrome c (Cytc), BCL2‐associated X, apoptosis regulator, poly ADP‐ribose polymerase (PARP), Cleave‐PARP, Caspase 9, autophagy immunoblot kit (LC3), and Beclin1 increased. Our research shows that PS‐MPs can trigger oxidative stress and induce cell cycle arrest, apoptosis, and autophagy in CIK cells by regulating ROS. This work provides a theoretical basis for cellular biology and toxicology mechanisms and new insights into the potential risks to animals from MPs exposure in the environment.

show abstract

“…ROS levels were detected using an ROS test kit (Nanjing Jiancheng Technology Company, China, E004-1-1). 46 The DCFH-DA probe was used in this experiment. The fluorescence images were observed by fluorescence microscopy.…”

Section: Ao/ebmentioning

confidence: 99%

1,4-Naphthoquinone-Coated Black Carbon, a Kind of Atmospheric Fine Particulate Matter, Affects Macrophage Fate: New Insights into Crosstalk between Necroptosis and Macrophage Extracellular Traps

Cui

Xiao

Yuan

et al. 2023

Environ. Sci. Technol.

View full text Add to dashboard Cite

1,4-Naphthoquinone-coated BC (1,4 NQ-BC) is an important component of PM2.5 and a representative secondary particle. However, there is no research on the crosstalk mechanism between necroptosis and macrophage extracellular traps (METs) after 1,4 NQ-BC exposure. In this study, we treated RAW264.7 cells with 50, 100, and 200 mg/L 1,4 NQ-BC for 24 h, with 10 μM necrostatin-1 for 24 h, and with 2.5 μM phorbol 12-myristate 13-acetate (PMA) for 3 h. Our experiment revealed that under normal physiological conditions, when macrophages receive external stimuli (such as pathogens; in this experiment, PMA), they will form METs and capture and kill pathogens, thus exerting innate immune function. However, exposure to 1,4 NQ-BC can cause necroptosis in macrophages, accompanied by increased levels of reactive oxygen species (ROS) and cytosolic calcium ions, as well as the expression disorder of inflammatory factors and chemokines, prevent the formation of METs, lead to loss of the function of capturing and killing pathogens, and weaken the innate immune function. Notably, inhibition of necroptosis restored the formation of METs, indicating that necroptosis inhibited the formation of METs. Our study was the first to explore the crosstalk mechanism between necroptosis and METs. This experiment will enrich the mechanism of macrophage injury caused by 1,4 NQ-BC exposure.

show abstract

ROS-mediated PPAR/RXR inhibition contributes to acetochlor-induced apoptosis and autophagy in Ctenopharyngodon idella hepatic cells

Cited by 51 publications

References 60 publications

Decreased thioredoxin reductase 3 expression promotes nickel‐induced damage to cardiac tissue via activating oxidative stress‐induced apoptosis and inflammation

Decreased thioredoxin reductase 3 expression promotes nickel‐induced damage to cardiac tissue via activating oxidative stress‐induced apoptosis and inflammation

Polystyrene microplastics mediate cell cycle arrest, apoptosis, and autophagy in the G2/M phase through ROS in grass carp kidney cells

1,4-Naphthoquinone-Coated Black Carbon, a Kind of Atmospheric Fine Particulate Matter, Affects Macrophage Fate: New Insights into Crosstalk between Necroptosis and Macrophage Extracellular Traps

Contact Info

Product

Resources

About