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

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 metal copper stress article environmental science beclin1-driven autophagy modulates copper induces apoptosis endoplasmic reticulum stress induces oxidative stress copper-induced pyroptosis mammalian endoplasmic reticulum pollution research aims full article pdf endoplasmic reticulum homeostasis jiangxi agricultural university privacy choices/manage cookies unfolded protein response inflammation-induced apoptosis modulating oxidative stress jianying guo supervised phthalate-induced pyroptosis protein quality control ire1alpha-xbp1 pathway beldean-galea ms tissue copper concentrations kilembe copper mine tribasic copper chloride cadmium-induced mitophagy cadmium-induced ferroptosis sertoli cell protects sh-sy5y cells liver copper concentrations particulate air pollution induce oxidative stress er quality control chronic copper toxicity holds exclusive rights domestic water quality regulating oxidative stress perturbed nerve fibers chinese mitten crab eriocheir japonica sinensis lycopene ameliorates di ei-emam ha

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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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