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

Atrazine exposure induces necroptosis through the P450/ROS pathway and causes inflammation in the gill of common carp (Cyprinus carpioL.).

Selenium (Se) is an antioxidant and immunomodulator that can participate in the control of specific endocrine pathways. Disturbance of redox homeostasis is closely related to the pathogenesis of many diseases. Se is also an important nutrient element for dairy cows. First, oxidative stress (OS) induced by Se deficiency was investigated along with a possible mechanism of its induction of mammary gland inflammation. This investigation used in vivo and in vitro experiments for verification. Once the OS response was triggered, the activity of antioxidant enzymes was reduced by regulation of the concentration of Se, which led to the accumulation of ROS. TNF-α, IL-1β, and IL-6 secretion was promoted to activate the NF-κB/MAPK signaling pathway. This process further promoted the accumulation of cytokines that aggravated the inflammatory response. Herein, it was verified that Se deficiency induces OS, which leads to ROS accumulation and the secretion of inflammatory factors to activate the NF-κB/MAPK signaling pathway and promote the occurrence of mastitis.

Selenium Deficiency Promotes Oxidative Stress-Induced Mastitis via Activating the NF-κB and MAPK Pathways in Dairy Cow

Deoxynivalenol induces carp neutrophil apoptosis and necroptosis via CYP450s/ROS/PI3K/AKT pathway

TMT induces apoptosis and necroptosis in mouse kidneys through oxidative stress-induced activation of the NLRP3 inflammasome

New insights into crosstalk between apoptosis and necroptosis co-induced by chlorothalonil and imidacloprid in Ctenopharyngodon idellus kidney cells.

Subacute cadmium exposure promotes M1 macrophage polarization through oxidative stress-evoked inflammatory response and induces porcine adrenal fibrosis.

Resveratrol relieves chlorothalonil-induced apoptosis and necroptosis through miR-15a/Bcl2-A20 axis in fish kidney cells.

Selenium (Se) is one of the essential trace elements; its deficiency induces ROS production and cell death in cardiomyocytes, skeletal muscle cells, and vascular smooth muscle cells, but it is still not clear the impact of Se deficiency on human uterine smooth muscle cells (HUSMCs). To investigate the effect of low Se on the mRNA expression of selenoproteins, the mRNA and protein expression of apoptosis and necroptosis of HUSMCs and their mechanism, Se deficient HUSMCs mode was established through culturing with 1% FBS containing 0 ng/mL, 0.7 ng/mL, and 7 ng/mL Se, and 10% FBS was as the control group. Then, the apoptosis and necroptosis rates, intracellular ROS content and the expression levels of selenoproteins, apoptosis, necroptosis, MAPK pathway-related genes were examined under different Se concentrations. The results showed that Se deficiency led to the augment of cell apoptosis and necroptosis in HUSMCs (p < 0.05), downregulated (p < 0.05) 19 selenoproteins (GPX1, GPX2, GPX3, GPX4, GPX6, Dio3, Txnrd2, Txnrd3, SEPHS2, SEL15, SELH, SELI, SELM, SELN, SELO, SELS, SELT, SELV, and SELW), while Dio2, SELK, Txnrd1, and MSRB1 were not affected by Se deficiency (p ≥ 0.05). In addition, Se deficiency led to increased intracellular ROS content, p-P38 and p-JNK gene expression levels (p < 0.05), the mitochondrial apoptosis pathway Bax, Casp9 and Cle-Casp3 protein expression levels (p < 0.05), and decreased Bcl2 protein expression level (p < 0.05), simultaneously, increased necroptosis marker genes RIP1, RIP3, and MLKL protein expression levels (p < 0.05) with a dose-dependent pattern. The above results indicate that Se deficiency induces HUSMCs apoptosis and necroptosis through the ROS/MAPK pathway and is closely related to selenoproteins.

Yujie Yao

Papers

New insights into crosstalk between apoptosis and necroptosis co-induced by chlorothalonil and imidacloprid in Ctenopharyngodon idellus kidney cells.

Subacute cadmium exposure promotes M1 macrophage polarization through oxidative stress-evoked inflammatory response and induces porcine adrenal fibrosis.

Resveratrol relieves chlorothalonil-induced apoptosis and necroptosis through miR-15a/Bcl2-A20 axis in fish kidney cells.

Selenium Deficiency Induces Apoptosis and Necroptosis Through ROS/MAPK Signal in Human Uterine Smooth Muscle Cells