Exposure to imidacloprid induce oxidative stress, mitochondrial dysfunction, inflammation, apoptosis and mitophagy via NF-kappaB/JNK pathway in grass carp hepatocytes

Selenoprotein K protects skeletal muscle from damage and is required for satellite cells-mediated myogenic differentiation

“…In a cardiotoxin-induced TA muscle injury model, genetic ablation of Nrf2 impaired antioxidant gene expression and sustained the burden of ROS, displaying immature and smaller TA muscle fibers compared to their WT counterparts [ 54 ]. Meanwhile, extensive evidence has shown that excessive ROS initiates apoptosis and autophagy in multiple physiological or pathological conditions [ [55] , [56] , [57] ]. Similar to most selenoproteins, SelK has been reported to regulate the balance of cellular redox.…”

The antagonistic effect of melatonin onTBBPA‐induced apoptosis and necroptosis viaPTEN/PI3K/AKTsignaling pathway in swine testis cells

“…It is well known that the principal mechanism of cytotoxicity leading to cell death is the excessive generation of ROS 39,40 . In this study, TBBPA increased the ROS level, and the imbalance of the antioxidant system activated oxidative stress in ST cells, leading to cell death.…”

“…38 Our research investigated the effect of TBBPA in ST cells and whether MT attenuates TBBPA- It is well known that the principal mechanism of cytotoxicity leading to cell death is the excessive generation of ROS. 39,40 In this study,…”

Bisphenol A aggravates renal apoptosis and necroptosis in selenium‐deficient chickens via oxidative stress and PI3K/AKT pathway

“…Oxidative stress is initially produced by accumulation of reactive oxygen species (ROS) and the imbalance of the antioxidant capacity in organisms. Toxic exposure can induce oxidative stress (Miao et al, 2022; Y. Wang, Zhao et al, 2021), and further oxidative stress triggers various signaling pathways, resulting in disturbed cellular ion homeostasis, inflammatory responses, apoptosis, and necroptosis (Gao et al, 2021; Samimi et al, 2019; H. Zhao et al, 2021), of which, it is worth noting that phosphatidylinositol 3‐kinase/threonine kinase (PI3K/AKT) signaling pathway, toxic exposure‐caused oxidative stress could downregulate PI3K/AKT signaling pathway (L. X. Li et al, 2022), leading to apoptosis through B‐cell lymphoma‐2 (Bcl‐2) signaling pathway, as well as programmed necroptosis via receptor‐interacting protein kinase 1 (RIP1)/RIP3/mixed lineage kinase domain‐like protein (MLKL) signaling pathway (L. Liu et al, 2021; L. Wang et al, 2020b). K. Li et al (2020) exposed chicken to ochratoxin A, finding that ochratoxin A induced renal apoptosis via modulation of oxidative stress and PI3K/AKT signaling pathway, and J. Zhang et al (2020) found that cadmium‐induced oxidative stress in common carp lymphocytes and promoted apoptosis and necrosis through the regulation of the miR‐216a‐PI3K/AKT axis, and pesticides chlorpyrifos induced the apoptosis and necroptosis in L8824 cells through the ROS/PTEN/PI3K/AKT axis (L. Wang et al, 2020b).…”

“…Oxidative stress is initially produced by accumulation of reactive oxygen species (ROS) and the imbalance of the antioxidant capacity in organisms. Toxic exposure can induce oxidative stress (Miao et al, 2022;, and further oxidative stress triggers various signaling pathways, resulting in disturbed cellular ion homeostasis, inflammatory responses, apoptosis, and necroptosis (Gao et al, 2021;Samimi et al, 2019;, of which, it is worth noting that phosphatidylinositol 3-kinase/threonine kinase (PI3K/AKT) signaling pathway, toxic exposure-caused oxidative stress could downregulate PI3K/AKT signaling pathway (L. X. Li et al, 2022), leading to apoptosis through B-cell lymphoma-2 (Bcl-2) signaling pathway, as well as programmed necroptosis via receptorinteracting protein kinase 1 (RIP1)/RIP3/mixed lineage kinase domain-like protein (MLKL) signaling pathway (L. Liu et al, 2021;L.…”