In vivo assessment of molybdenum and cadmium co-induce nephrotoxicity via causing calcium homeostasis disorder and autophagy in ducks (Anas platyrhyncha)

Zhang, Caiying; Lin, Tianjin; Nie, Guoxing; Hu, Ruiming; Pi, Shaoxing; Wei, Zejing; Wang, Chang; Li, Guyue; Hu, Guoliang

doi:10.1016/j.ecoenv.2021.113099

Cited by 27 publications

(19 citation statements)

References 44 publications

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“…78 With the gradual loss of ER function, ER will further release Ca 2+ into the cell cytoplasm. 79 High concentrations of Ca 2+ can directly act on mitochondria, causing mitochondrial dysfunction and triggering mitochondrial-related apoptosis. 80 However, the effect of DLM on intracellular Ca 2+ in cells of quail has not been reported to date.…”

Section: Discussionmentioning

confidence: 99%

“…The response of ER stress will produce a large amount of CHOP, which inhibits the expression of Bcl‐2 located on the mitochondrial membrane, thereby promoting apoptosis of the mitochondrial pathway 78 . With the gradual loss of ER function, ER will further release Ca 2+ into the cell cytoplasm 79 . High concentrations of Ca 2+ can directly act on mitochondria, causing mitochondrial dysfunction and triggering mitochondrial‐related apoptosis 80 .…”

Section: Discussionmentioning

confidence: 99%

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Deltamethrin induces apoptosis in cerebrum neurons of quail via promoting endoplasmic reticulum stress and mitochondrial dysfunction

Han

et al. 2022

Environmental Toxicology

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Deltamethrin (DLM) is a widely used and highly effective insecticide. DLM exposure is harmful to animal and human. Quail, as a bird model, has been widely used in the field of toxicology. However, there is little information available in the literature about quail cerebrum damage caused by DLM. Here, we investigated the effect of DLM on quail cerebrum neurons. Four groups of healthy quails were assigned (10 quails in each group), respectively given 0, 15, 30, and 45 mg/kg DLM by gavage for 12 weeks. Through the measurements of quail cerebrum, it was found that DLM exposure induced obvious histological changes, oxidative stress, and neurons apoptosis. To further explore the possible molecular mechanisms, we performed real-time quantitative PCR to detect the expression of endoplasmic reticulum (ER) stressrelated mRNA such as glucose regulated protein 78 kD, activating transcription factor 6, inositol requiring enzyme, and protein kinase RNA (PKR)-like ER kinase. In addition, we detected ATP content in quail cerebrum to evaluate the functional status of mitochondria. The study showed that DLM exposure significantly increased the expression of ER stress-related mRNA and decreased ATP content in quail cerebrum tissues. These results suggest that chronic exposure to DLM induces apoptosis of quail cerebrum neurons via promoting ER stress and mitochondrial dysfunction. Furthermore, our results provide a novel explanation for DLM-induced apoptosis of avian cerebrum neurons.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Deltamethrin induces apoptosis in cerebrum neurons of quail via promoting endoplasmic reticulum stress and mitochondrial dysfunction

Han

et al. 2022

Environmental Toxicology

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“…Se is a crucial component of many enzymes and antioxidants. When combined with proteins, it can exert a wide range of multi-effect roles, such as anti-oxidation and anti-inflammation [ 50 , 51 ]. According to our results, Cd caused the accumulation of ROS, decreased the levels of GSH-Px, SOD and T-AOC, and elevated the content of MDA, and Se could reverse the above changes, which proved that Cd caused oxidative stress in hepatocytes, and Se could antagonize oxidative stress caused by Cd.…”

Section: Discussionmentioning

confidence: 99%

“…With reference to quondam investigation [ 51 ], the cells were cultured with rabbit anti-HMGB1 antibody (1:300) for 12 h and goat anti-rabbit antibody (1:500) for 1 h. The immunofluorescence of HMGB1 was imaged and analyzed with a confocal fluorescence microscope (TCS SP8; Leica, Wetzlar, Germany).…”

Section: Methodsmentioning

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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“…The sample immersed in 4% paraformaldehyde solution was stained with hematoxylin and eosin (HE), 39 oil‐red O, and Masson trichrome staining, 40,41 respectively, and observed with a common optical microscope (BX‐FM: Olympus Corp, Tokyo, Japan). The liver pathology score was divided into 0–4.…”

Section: Methodsmentioning

confidence: 99%

Inhibition of the Nrf2 signaling pathway involved in imidacloprid‐induced liver fibrosis in Coturnix japonica

Deng

Bing

et al. 2022

Environmental Toxicology

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Imidacloprid (IMI) is a kind of widely used neonicotinoid insecticide. However, the toxicity of IMI is not only applied to target pests but also causes serious negative effects on birds and other creatures. Our previous studies have shown that long‐term exposure to IMI can induce liver fibrosis in quails. However, the specific mechanism of quail liver fibrosis induced by IMI is not completely clear. Accordingly, the purpose of this study is to further clarify the potential molecular mechanism of IMI‐induced liver fibrosis in quails. Japanese quails (Coturnix japonica) were treated with/without IMI (intragastric administration with 6 mg/kg body weight) in the presence/absence of luteolin (Lut) (fed with 800 mg/kg) for 90 days. The results reveal that IMI can induce hepatic fibrosis, oxidative stress, fatty degeneration, inflammation, and the down‐expression of nuclear factor‐E2‐related factor‐2 (Nrf2). Furthermore, the treatment of Lut, a kind of Nrf2 activator, increased the expression of Nrf2 in livers and alleviated liver fibrosis in quails. Altogether, our study demonstrates that inhibition of the Nrf2 pathway is the key to liver fibrosis induced by IMI in quails. These results provide a new understanding for the study of the toxicity of IMI and a practical basis for the treatment of liver fibrosis caused by IMI.

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In vivo assessment of molybdenum and cadmium co-induce nephrotoxicity via causing calcium homeostasis disorder and autophagy in ducks (Anas platyrhyncha)

Cited by 27 publications

References 44 publications

Deltamethrin induces apoptosis in cerebrum neurons of quail via promoting endoplasmic reticulum stress and mitochondrial dysfunction

Deltamethrin induces apoptosis in cerebrum neurons of quail via promoting endoplasmic reticulum stress and mitochondrial dysfunction

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

Inhibition of the Nrf2 signaling pathway involved in imidacloprid‐induced liver fibrosis in Coturnix japonica

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