Molybdenum and cadmium co-exposure induces endoplasmic reticulum stress-mediated apoptosis by Th1 polarization in Shaoxing duck (Anas platyrhyncha) spleens

Guo, Huiling; Hu, Ruiming; Huang, Gang; Pu, Wenjing; Chu, Xuesheng; Xing, Chenghong; Zhang, Caiying

doi:10.1016/j.chemosphere.2022.134275

Cited by 27 publications

(15 citation statements)

References 61 publications

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“…Liu et al proved that exposure to amorphous SiO2 NP could promote the release of HMGB1 from the nucleus to the cytoplasm, thus activating the NF-κB signaling pathway, leading to inflammatory injury of human umbilical vein endothelial cells (HUVEC) [ 21 ]. Recent studies have shown that Cd can produce a series of adverse effects, including increasing autophagy levels and promoting apoptosis, endoplasmic reticulum stress and pyroptosis in vivo or in vitro experimental models [ 22 , 23 , 24 , 25 ]. Furthermore, these undesirable reactions are accompanied by the addition of inflammatory cytokines and the enhancement of inflammatory levels.…”

Section: Introductionmentioning

confidence: 99%

Selenium Antagonizes Cadmium-Induced Inflammation and Oxidative Stress via Suppressing the Interplay between NLRP3 Inflammasome and HMGB1/NF-κB Pathway in Duck Hepatocytes

Cao

Yang

Lin

et al. 2022

IJMS

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Cadmium (Cd) is a toxic heavy metal that can accumulate in the liver of animals, damaging liver function. Inflammation and oxidative stress are considered primary causes of Cd-induced liver damage. Selenium (Se) is an antioxidant and can resist the detrimental impacts of Cd on the liver. To elucidate the antagonism of Se on Cd against hepatocyte injury and its mechanism, duck embryo hepatocytes were treated with Cd (4 μM) and/or Se (0.4 μM) for 24 h. Then, the hepatocyte viability, oxidative stress and inflammatory status were assessed. The findings manifested that the accumulation of reactive oxygen species (ROS) and the levels of pro-inflammatory factors were elevated in the Cd group. Simultaneously, immunofluorescence staining revealed that the interaction between NOD-like receptor pyran domain containing 3 (NLRP3) and apoptosis-associated speck-like protein (ASC) was enhanced, the movement of high-mobility group box 1 (HMGB1) from nucleus to cytoplasm was increased and the inflammatory response was further amplified. Nevertheless, the addition of Se relieved the above-mentioned effects, thereby alleviating cellular oxidative stress and inflammation. Collectively, the results suggested that Se could mitigate Cd-stimulated oxidative stress and inflammation in hepatocytes, which might be correlated with the NLRP3 inflammasome and HMGB1/nuclear factor-κB (NF-κB) signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Selenium Antagonizes Cadmium-Induced Inflammation and Oxidative Stress via Suppressing the Interplay between NLRP3 Inflammasome and HMGB1/NF-κB Pathway in Duck Hepatocytes

Cao

Yang

Lin

et al. 2022

IJMS

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“…Overall, ER stress benefits cellular survival by inducing autophagy; however, prolonged ER stress can induce cellular death and damage [ 45 ]. Many studies have indicated that heavy metal-induced ER stress mediates cell death by affecting autophagy-related signaling [ 46 , 47 ].…”

Section: The Signaling Pathways Of Autophagymentioning

confidence: 99%

The Effect of Oxidative Stress-Induced Autophagy by Cadmium Exposure in Kidney, Liver, and Bone Damage, and Neurotoxicity

Yue

et al. 2022

IJMS

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Environmental and occupational exposure to cadmium has been shown to induce kidney damage, liver injury, neurodegenerative disease, and osteoporosis. However, the mechanism by which cadmium induces autophagy in these diseases remains unclear. Studies have shown that cadmium is an effective inducer of oxidative stress, DNA damage, ER stress, and autophagy, which are thought to be adaptive stress responses that allow cells exposed to cadmium to survive in an adverse environment. However, excessive stress will cause tissue damage by inducing apoptosis, pyroptosis, and ferroptosis. Evidently, oxidative stress-induced autophagy plays different roles in low- or high-dose cadmium exposure-induced cell damage, either causing apoptosis, pyroptosis, and ferroptosis or inducing cell survival. Meanwhile, different cell types have different sensitivities to cadmium, which ultimately determines the fate of the cell. In this review, we provided a detailed survey of the current literature on autophagy in cadmium-induced tissue damage. A better understanding of the complex regulation of cell death by autophagy might contribute to the development of novel preventive and therapeutic strategies to treat acute and chronic cadmium toxicity.

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“…Excess Mo enters and cumulates in the body, and finally produces toxic effects 3 . Studies have revealed that Mo can cause immunotoxicity in avian 6,7 . Multiple researches have affirmed that excess amounts of Mo cause oxidative stress, autophagy and pyroptosis in spleen, liver and kidney 7–9 …”

Section: Introductionmentioning

confidence: 99%

“…3 Studies have revealed that Mo can cause immunotoxicity in avian. 6,7 Multiple researches have affirmed that excess amounts of Mo cause oxidative stress, autophagy and pyroptosis in spleen, liver and kidney. [7][8][9] Cadmium (Cd) is an omnipresent environmental contaminant and is regarded as the seventh category of toxic heavy metal, posing a significant hazard to human and animal health.…”

Section: Introductionmentioning

confidence: 99%

“…6,7 Multiple researches have affirmed that excess amounts of Mo cause oxidative stress, autophagy and pyroptosis in spleen, liver and kidney. [7][8][9] Cadmium (Cd) is an omnipresent environmental contaminant and is regarded as the seventh category of toxic heavy metal, posing a significant hazard to human and animal health. 10,11 It is derived not only from volcanic activity, forest fires and mining 12,13 but also from corrosive reagents, stabilizers in PVC products, color pigments, and nickel-Cd batteries, which increases its deposition in the environment and risk of its enrichment in animals.…”

Section: Introductionmentioning

confidence: 99%

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Co‐exposure to molybdenum and cadmium triggers pyroptosis and autophagy byPI3K/AKTaxis in duck spleens

Chu

Dai

et al. 2022

Environmental Toxicology

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Excessive amounts of molybdenum (Mo) and cadmium (Cd) are toxicant, but their combined immunotoxicity are not clearly understood. To estimate united impacts of Mo and Cd on pyroptosis and autophagy by PI3K/AKT axis in duck spleens, Mo or/and Cd subchronic toxicity models of ducks were established by feeding diets with different dosages of Mo or/and Cd. Data show that Mo or/and Cd cause oxidative stress by increasing MDA concentration, and decreasing T-AOC, CAT, GSH-Px and T-SOD activities, restrain PI3K/AKT axis by decreasing PI3K, AKT, p-AKT expression levels, which evokes pyroptosis and autophagy by elevating IL-1β, IL-18 concentrations and NLRP3, Caspase-1, ASC, GSDME, GSDMA, NEK7, IL-1β, IL-18 expression levels, promoting autophagosomes, LC3 puncta, Atg5, LC3A, LC3B, LC3II/LC3I and Beclin-1 expression levels, and reducing expression levels of P62 and Dynein. Furthermore, the variations of abovementioned indexes are most pronounced in co-treated group. Overall, results reveal that Mo or/and Cd may evoke pyroptosis and autophagy by PI3K/AKT axis in duck spleens. The association of Mo and Cd exacerbates the changes.

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Molybdenum and cadmium co-exposure induces endoplasmic reticulum stress-mediated apoptosis by Th1 polarization in Shaoxing duck (Anas platyrhyncha) spleens

Cited by 27 publications

References 61 publications

Selenium Antagonizes Cadmium-Induced Inflammation and Oxidative Stress via Suppressing the Interplay between NLRP3 Inflammasome and HMGB1/NF-κB Pathway in Duck Hepatocytes

Selenium Antagonizes Cadmium-Induced Inflammation and Oxidative Stress via Suppressing the Interplay between NLRP3 Inflammasome and HMGB1/NF-κB Pathway in Duck Hepatocytes

The Effect of Oxidative Stress-Induced Autophagy by Cadmium Exposure in Kidney, Liver, and Bone Damage, and Neurotoxicity

Co‐exposure to molybdenum and cadmium triggers pyroptosis and autophagy byPI3K/AKTaxis in duck spleens

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