We are analyzing https://link.springer.com/article/10.1007/s11356-023-29397-6.

Title:
Toxic effects of copper on duck cerebrum: a crucial role of oxidative stress and endoplasmic reticulum quality control | Environmental Science and Pollution Research
Description:
To study the effects of Cu overload on ER quality control in duck cerebrums, 144 ducks were treated with 8 mg/kg, 100 mg/kg, 200 mg/kg and 400 mg/kg Cu added in the feed for 45 days. From histopathological examination, we found that excessive Cu increased the amount of microglia and disintegrated neuron, decreased the number of Nissl bodies, perturbed nerve fibers in duck cerebrums. Cu poisoning also increased Cu, H2O2, T-SOD, and MDA levels, decreased Fe and CAT contents in duck cerebrums. Furthermore, Cu treatment upregulated the mRNA levels of the unfolded protein response genes (PERK, ATF6, and IRE1), ER-associated degradation genes (CNX, Derlin1, and Derlin2), autophagy genes (ATG5, ATG7, ATG10, Beclin1, LC3A, LC3B, and P62), and heat shock response genes (Hsp70 and Hsp90) in duck cerebrums; elevated the protein levels of p-PERK, CNX, SEL1L, Beclin1, P62, and LC3BII/LC3BI in duck cerebrums; increased the numbers of SEL1L and LC3B puncta in duck cerebrums. Thus, our data showed that excessive Cu could cause histopathological damage to duck cerebrums, disrupt the balance of the trace elements, induce oxidative stress and activation of ER quality control, thereby resulting in duck cerebrums damage.
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Keywords {🔍}

article, google, scholar, cas, wang, stress, copper, endoplasmic, yang, zhang, oxidative, reticulum, duck, environ, sci, liu, guo, autophagy, quality, control, cerebrums, response, data, research, trace, cao, science, effects, fan, author, biol, pathway, xing, han, res, jiangxi, privacy, cookies, manuscript, huo, protein, disease, cell, httpsdoiorgs, copperinduced, apoptosis, cells, induces, chicken, pollut,

Topics {✒️}

perk/atf4/chop signaling pathway month download article/chapter metal-induced oxidative stress pi3k/akt/pten signaling sirt1/hsf1/hsp pathway endoplasmic stress-ferritinophagy axis cadmium-induced cardiac injury copper-induced oxidative stress classic caspase-1/nlrp3 pathway article environmental science beclin1-driven autophagy modulates endoplasmic reticulum stress mammalian endoplasmic reticulum endoplasmic reticulum homeostasis copper induces apoptosis pollution research aims full article pdf jiangxi agricultural university privacy choices/manage cookies unfolded protein response copper-induced pyroptosis modulating oxidative stress inflammation-induced apoptosis jianying guo supervised cadmium-induced mitophagy induces oxidative stress protein quality control ire1alpha-xbp1 pathway beldean-galea ms phthalate-induced pyroptosis tissue copper concentrations cadmium-induced ferroptosis kilembe copper mine tribasic copper chloride particulate air pollution induce oxidative stress er quality control sertoli cell protects liver copper concentrations holds exclusive rights regulating oxidative stress chronic copper toxicity domestic water quality perturbed nerve fibers lycopene ameliorates di ei-emam ha priority pollutants present ischemic stroke hospitalization revised paper process abdel-daim publisher

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         description:To study the effects of Cu overload on ER quality control in duck cerebrums, 144 ducks were treated with 8 mg/kg, 100 mg/kg, 200 mg/kg and 400 mg/kg Cu added in the feed for 45 days. From histopathological examination, we found that excessive Cu increased the amount of microglia and disintegrated neuron, decreased the number of Nissl bodies, perturbed nerve fibers in duck cerebrums. Cu poisoning also increased Cu, H2O2, T-SOD, and MDA levels, decreased Fe and CAT contents in duck cerebrums. Furthermore, Cu treatment upregulated the mRNA levels of the unfolded protein response genes (PERK, ATF6, and IRE1), ER-associated degradation genes (CNX, Derlin1, and Derlin2), autophagy genes (ATG5, ATG7, ATG10, Beclin1, LC3A, LC3B, and P62), and heat shock response genes (Hsp70 and Hsp90) in duck cerebrums; elevated the protein levels of p-PERK, CNX, SEL1L, Beclin1, P62, and LC3BII/LC3BI in duck cerebrums; increased the numbers of SEL1L and LC3B puncta in duck cerebrums. Thus, our data showed that excessive Cu could cause histopathological damage to duck cerebrums, disrupt the balance of the trace elements, induce oxidative stress and activation of ER quality control, thereby resulting in duck cerebrums damage.
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      description:To study the effects of Cu overload on ER quality control in duck cerebrums, 144 ducks were treated with 8 mg/kg, 100 mg/kg, 200 mg/kg and 400 mg/kg Cu added in the feed for 45 days. From histopathological examination, we found that excessive Cu increased the amount of microglia and disintegrated neuron, decreased the number of Nissl bodies, perturbed nerve fibers in duck cerebrums. Cu poisoning also increased Cu, H2O2, T-SOD, and MDA levels, decreased Fe and CAT contents in duck cerebrums. Furthermore, Cu treatment upregulated the mRNA levels of the unfolded protein response genes (PERK, ATF6, and IRE1), ER-associated degradation genes (CNX, Derlin1, and Derlin2), autophagy genes (ATG5, ATG7, ATG10, Beclin1, LC3A, LC3B, and P62), and heat shock response genes (Hsp70 and Hsp90) in duck cerebrums; elevated the protein levels of p-PERK, CNX, SEL1L, Beclin1, P62, and LC3BII/LC3BI in duck cerebrums; increased the numbers of SEL1L and LC3B puncta in duck cerebrums. Thus, our data showed that excessive Cu could cause histopathological damage to duck cerebrums, disrupt the balance of the trace elements, induce oxidative stress and activation of ER quality control, thereby resulting in duck cerebrums damage.
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