Selenium ameliorates mercuric chloride-induced brain damage through activating BDNF/TrKB/PI3K/AKT and inhibiting NF-κB signaling pathways

Li, Lanxin; Chu, Jia-Hong; Chen, Xuewei; Gao, Pei-Chao; Wang, Zhenyong; Liu, Ci; Fan, Rui-Feng

doi:10.1016/j.jinorgbio.2022.111716

Cited by 40 publications

(13 citation statements)

References 51 publications

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“…Vitamin E could have a role in forming selenium mercury complexes in tissues, decreasing mercury toxicity, primarily by reducing mercury absorption through the elementary canal ( Uzunhisarcikli et al., 2015 ). Also, selenium antagonizes mercury toxicity in the brain of chickens by promoting the signaling pathways BDNF/TrKB/PI3K/AKT and suppressing NF-kappaB ( Li et al., 2022 ). It reduces the liver damage caused by mercuric chloride by controlling mitochondrial dynamics to prevent the interaction between energy metabolism dysfunction and NF–B/NLRP3 inflammasome-mediated inflammation ( Gao et al., 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Amelioration of mercuric chloride-induced physiologic and histopathologic alterations in rats using vitamin E and zinc chloride supplement

Shalan

2022

Heliyon

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Section: Discussionmentioning

confidence: 99%

Amelioration of mercuric chloride-induced physiologic and histopathologic alterations in rats using vitamin E and zinc chloride supplement

Shalan

2022

Heliyon

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“…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).…”

Section: Introductionmentioning

confidence: 99%

“…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. Wang et al, 2020b).…”

mentioning

confidence: 99%

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

Chen

Zhang

Zou

et al. 2022

Journal Cellular Physiology

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Bisphenol A (BPA) in the environment can have deleterious effects on humans and animals. BPA can exert nephrotoxicity by inducing oxidative stress. Selenium (Se) deficiency can specifically impair kidney tissues and additionally show a synergistic effect on the toxicity of several environmental chemicals. However, the toxic effects of BPA on the chicken kidney and whether Se deficiency produces synergistic effects on the toxicity of BPA remain poorly understood. Herein, we established BPA exposure models and Se deficiency model in vivo and in vitro, and described the discovery path of BPA aggravation on apoptosis and necroptosis in Se-deficient chicken kidneys via regulation of oxidative stress and phosphatidylinositol 3-kinase/ threonine kinase (PI3K/AKT) signaling pathway. We found that BPA exposure increased reactive oxygen species and malondialdehyde levels, reduced activities of catalase, GPx, and superoxide dismutase, downregulated PI3K and AKT expressions, activated Bcl/Bax-Caspase 9-Caspase 3, and receptor-interacting protein kinase 1/mixed lineage kinase domain-like protein signaling pathways, resulting in apoptosis and necroptosis in the chicken kidney. In addition, Se deficiency significantly promoted the expression of renal apoptosis and necroptosis in BPA-exposed chicken kidneys. Altogether, our results showed that BPA aggravates apoptosis and necroptosis in Sedeficient chicken kidneys via regulation of oxidative stress and PI3K/AKT signaling pathway. Our findings elucidate the mechanism of BPA nephrotoxicity and Se deficiency exacerbation toxicity in chickens and will provide great significance for the protection of the ecological environment and animal health.

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“…38 Studies have shown that cytokines TNF-α and IL-1β can regulate immune function and activate JNK and P38 signaling pathways. [39][40][41][42] Resveratrol is (RSV, 3, 4 0 ,5-trihydroxy-1,2-diphenylethylene) a natural non-flavonoid polyphenolic organic compound with potent antioxidant and anti-inflammatory activities. 43 RSV enhances lung antioxidant effects in chicken heat stress-induced lung injury models by activating the Nrf2 pathway and autophagy.…”

mentioning

confidence: 99%

Resveratrol alleviates imidacloprid‐induced mitochondrial apoptosis, necroptosis, and immune dysfunction in chicken lymphocyte lines by inhibiting the ROS/MAPK signaling pathway

Wang,

Sun,

et al. 2023

Environmental Toxicology

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Imidacloprid (IMI) is a neonicotinoid insecticide with the highest global market share, and IMI exposure in the environment can negatively affect many nontarget organisms (a general term for organisms affected by drugs other than target organisms). Resveratrol (RSV), a non‐flavonoid polyphenolic organic compound derived from peanuts, grapes, and other plants, has anti‐inflammatory and antioxidant effects. It is currently unclear how RSV protects against cell damage caused by IMI. Therefore, we established an experimental model of chicken lymphocyte lines exposed to 110 μg/mL IMI and/or 0.5 μM RSV for 24 h. According to the experimental results, IMI markedly raised intracellular reactive oxygen species levels and diminished the activity of the cellular antioxidant enzymes (CAT, SOD, and GPx), leading to MDA accumulation and decreased T‐AOC. JNK, ERK, and P38, the essential components of the mitogen‐activated protein kinase (MAPK) signaling pathway, were also expressed more when IMI was present. Additionally, IMI resulted in upregulation of mitochondrial apoptosis (Caspase 3, Caspase 9, Bax, and Cyt‐c) and necroptosis (Caspase 8, RIPK1, RIPK3, and MLKL) related factors expression, downregulation of Bcl‐2 expression, induction of upregulation of cytokine IL‐6 and TNF‐α expression, and downregulation of IFN‐γ expression. The combined treatment of RSV and IMI significantly reduced cellular oxidative stress levels, inhibited the MAPK signaling pathway, and alleviated IMI‐induced mitochondrial apoptosis, necroptosis, and immune dysfunction. To summarize, RSV antagonized IMI‐induced mitochondrial apoptosis, necroptosis, and immune dysfunction in chicken lymphocyte lines by inhibiting the ROS/MAPK signaling pathway.

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Selenium ameliorates mercuric chloride-induced brain damage through activating BDNF/TrKB/PI3K/AKT and inhibiting NF-κB signaling pathways

Cited by 40 publications

References 51 publications

Amelioration of mercuric chloride-induced physiologic and histopathologic alterations in rats using vitamin E and zinc chloride supplement

Amelioration of mercuric chloride-induced physiologic and histopathologic alterations in rats using vitamin E and zinc chloride supplement

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

Resveratrol alleviates imidacloprid‐induced mitochondrial apoptosis, necroptosis, and immune dysfunction in chicken lymphocyte lines by inhibiting the ROS/MAPK signaling pathway

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