Cadmium Transforms Astrocytes into the A1 Subtype via Inducing Gap Junction Protein Connexin 43 into the Nucleus DOI
Yingxin Zhao,

Xue‐Nan Li,

Yi-Xi Tang

et al.

Journal of Agricultural and Food Chemistry, Journal Year: 2023, Volume and Issue: 71(31), P. 12043 - 12051

Published: July 20, 2023

Cadmium is highly toxic and present in the environment can be accumulated among various levels of food chain. Both humans animals are at risk from toxicity associated with cadmium. However, neurological endpoint caused by cadmium has not been revealed. The aim our research to explore potential target attack when causing neurotoxicity. 80 male chickens (one day old, weighing 36.49 ± 2.88 g) were randomly divided into four groups independently treated 0, 35, 70, or 140 mg/kg CdCl2 diet for 90 days. result showed that striatum was damaged due a high dose brain, which characterized degeneration neurons astrocyte dysfunction. Transcriptome analysis demonstrated striatal astrocytes transformed A1 state under exposure. Deeper investigation revealed internalization gap junction protein connexin 43 responsible this transformation. Eventually, we conclude internalized anchoring, process accompanied transformation subtype. This study provides new direction exploring effects on nervous system treatment subsequent diseases.

Language: Английский

Novel Role of Hemeoxygenase-1 in Phthalate-Induced Renal Proximal Tubule Cell Ferroptosis DOI
Ming‐Shan Chen, Jiaxin Wang, Hao Zhang

et al.

Journal of Agricultural and Food Chemistry, Journal Year: 2023, Volume and Issue: 71(5), P. 2579 - 2589

Published: Jan. 25, 2023

Phthalates are widely used to improve the flexibility of poly(vinyl chloride) (PVC) polymer agriculture products. Di(2-ethylhexyl) phthalate (DEHP) is a type addition plastic and can lead many health problems. Hemeoxygenase-1 (HO-1) an extremely important molecule that releases enzymatic products promote ferroptosis. This research aimed explore function HO-1 in DEHP-induced renal proximal tubule cell In experiment, ICR male mice exposed (0, 50, 200, 500 mg/kg BW/day) DEHP for 28 days. Here, we observed induced glomeruli atrophy tubules swell. Furthermore, exposure could increase ferrous iron content decrease antioxidant activity. We also found increased expression nuclear factor-erythroid 2 p45-related factor (NFE2L2) nucleus. particular, significantly both protein mRNA levels. Glutathione peroxidase 4 (GPX4) as endogenous control ferroptosis was downregulated, which proved occurrence study, activated NFE2L2/HO-1 signaling pathway resulted tubule. connects with HO-1, providing new insights into potential roles phthalates nephrotoxicity.

Language: Английский

Citations

18

Melatonin Mitigates Atrazine-Induced Renal Tubular Epithelial Cell Senescence by Promoting Parkin-Mediated Mitophagy DOI Creative Commons
Yu-Sheng Shi,

Tian‐Ning Yang,

Yuxiang Wang

et al.

Research, Journal Year: 2024, Volume and Issue: 7

Published: Jan. 1, 2024

The accumulation of senescent cells in kidneys is considered to contribute age-related diseases and organismal aging. Mitochondria are a regulator cell senescence process. Atrazine as triazine herbicide poses threat renal health by disrupting mitochondrial homeostasis. Melatonin plays critical role maintaining present study aims explore the mechanism which melatonin alleviates atrazine-induced injury whether parkin-mediated mitophagy contributes mitigating senescence. found that level parkin was decreased after atrazine exposure negatively correlated with markers. treatment increased serum levels mitigates tubular epithelial Mechanistically, maintains integrity crista structure increasing contact site cristae organizing system, transcription factor A (TFAM), adenosine triphosphatase family AAA domain-containing protein 3A (ATAD3A), sorting assembly machinery 50 (Sam50) prevent DNA release subsequent activation cyclic guanosine 5′-monophosphate–adenosine 5′-monophosphate synthase pathway. Furthermore, activates Sirtuin 3–superoxide dismutase 2 axis eliminate reactive oxygen species kidney. More importantly, antisenescence largely determined parkin-dependent mitophagy. These results offer novel insights into measures against Parkin-mediated promising drug target for alleviating

Language: Английский

Citations

7

Lycopene Prevents Phthalate-Induced Cognitive Impairment via Modulating Ferroptosis DOI
Haoran Wang,

Muzi Li,

Jia-Gen Cui

et al.

Journal of Agricultural and Food Chemistry, Journal Year: 2023, Volume and Issue: 71(44), P. 16727 - 16738

Published: Oct. 23, 2023

Di-(2-ethylhexyl) phthalate (DEHP) is frequently used as a plasticizer in industrial and agricultural products. DEHP can cause severe neurotoxicity, such impaired learning memory function. Lycopene (LYC) carotenoid exerts excellent antioxidant capacity therapeutic effects neurodegenerative diseases. However, whether LYC prevent the cognitive impairment induced by specific mechanisms are unclear. In present study, behavioral test results suggested that alleviated DEHP. The histopathological data revealed attenuated DEHP-induced disordered arrangement of neurons CA1 CA3 regions hippocampus tissue. Moreover, inhibited occurrence ferroptosis via regulating iron metabolism, inhibiting lipid peroxidation, activating cysteine transporter nuclear factor erythroid 2-related 2/heme oxygenase-1 (NrF2/HO-1) signaling pathway. Overall, study contributes novel perspectives into potential preventing phthalate-induced hippocampus.

Language: Английский

Citations

13

Inhibition of the p62-Nrf2-GPX4 Pathway Confers Sensitivity to Butachlor-Induced Splenic Macrophage Ferroptosis DOI
Yi Zhao,

Shang-Jia Yang,

Yifeng Huang

et al.

Journal of Agricultural and Food Chemistry, Journal Year: 2024, Volume and Issue: 72(30), P. 16998 - 17007

Published: July 17, 2024

Butachlor is widely used in agriculture around the world and therefore poses environmental public health hazards due to persistent poor biodegradability. Ferroptosis a type of iron-mediated cell death controlled by glutathione (GSH) GPX4 inhibition. P62 an essential autophagy adaptor that regulates Keap1 activate nuclear factor erythroid 2-related 2 (Nrf2), which effectively suppresses lipid peroxidation, thereby relieving ferroptosis. Here, we found butachlor caused changes splenic macrophage structure, especially impaired mitochondrial morphology with disordered suggestive occurrence This was further confirmed detection iron metabolism, GSH system, peroxidation. Mechanistically, suppressed protein level p62 promoted Keap1-mediated degradation Nrf2, results decreased expression accelerated These findings suggest targeting p62-Nrf2-GPX4 signaling axis may be promising strategy for treating inflammatory diseases.

Language: Английский

Citations

5

T-2 toxin induces cardiotoxicity by activating ferroptosis and inhibiting heme oxygenase-1 DOI
Chi Chiu Wang, Jun He, Jin Hong

et al.

Chemosphere, Journal Year: 2023, Volume and Issue: 341, P. 140087 - 140087

Published: Sept. 5, 2023

Language: Английский

Citations

11

Phthalate drives splenic inflammatory response via activating HSP60/TLR4/NLRP3 signaling axis-dependent pyroptosis DOI

Xinran Ge,

Yi Zhao,

Hao-Ran Ren

et al.

Environmental Pollution, Journal Year: 2024, Volume and Issue: 346, P. 123610 - 123610

Published: Feb. 19, 2024

Language: Английский

Citations

4

A review of photocatalytic CO2 reduction: exploring sustainable carbon emission mitigation from thermodynamics to kinetics and strategies for enhanced efficiency DOI

Hassan Akbar,

Muhammad Subhan Javed,

Syeda Tehreem Iqbal

et al.

Journal of the Korean Ceramic Society, Journal Year: 2024, Volume and Issue: 61(3), P. 367 - 390

Published: Feb. 21, 2024

Language: Английский

Citations

4

Cadmium targeting transcription factor EB to inhibit autophagy-lysosome function contributes to acute kidney injury DOI Creative Commons
Pengfei Dong,

Tian-Bin Liu,

Kai Chen

et al.

Journal of Advanced Research, Journal Year: 2024, Volume and Issue: unknown

Published: July 1, 2024

Environmental and occupational exposure to cadmium (Cd) has been shown cause acute kidney injury (AKI). Previous studies have demonstrated that autophagy inhibition lysosomal dysfunction are important mechanisms of Cd-induced AKI. Transcription factor EB (TFEB) is a critical transcription regulator modulates autophagy-lysosome function, but its role in AKI yet be elucidated. Thus, vivo vitro were conducted clarify this issue. Data firstly showed reduced TFEB expression nuclear translocation evident models, accompanied by dysfunction. Pharmacological genetic activation improved via alleviating dysfunction, whereas Tfeb knockdown further aggravated phenomenon, suggesting the key regulating autophagy. Mechanistically, Cd activated mechanistic target rapamycin complex 1 (mTORC1) enhance phosphorylation thereby inhibiting translocation. also chromosome region maintenance (CRM1) promote export. Meanwhile, general control non-repressed protein 5 (GCN5) acetylation, resulting decreased transcriptional activity. Moreover, CRM1 or GCN5 alleviated enhancing activity, respectively. In summary, these findings reveal phosphorylation, export acetylation independently suppress activity might promising treatment strategy for

Language: Английский

Citations

4

TNF/TNFR1 Signaling Mediates DEHP-Induced Hepatocyte Pyroptosis via the GSDMD–mtROS Axis DOI
Hao Zhang,

Jia-Gen Cui,

Ming‐Shan Chen

et al.

Journal of Agricultural and Food Chemistry, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 25, 2025

Di(2-ethylhexyl) phthalate (DEHP), which is widely used in agricultural plastics, accumulates humans and animals through the food chain over time, resulting liver toxicity. Recent studies have reported that pyroptosis mitochondrial damage are closely related to a variety of diseases, but specific mechanism still unclear. To address this issue, vitro vivo hepatotoxicity models were established. The results demonstrated exposure DEHP caused buildup MEHP livers, altered metabolite composition, pyroptosis-like changes hepatocytes. After treatment, REDOX homeostasis was unbalanced, reactive oxygen species (mtROS) overproduced. activates mediated by TNF/TNFR1 signaling upregulates perforating protein GSDMD-N destroy membrane Above all, study elucidates potential involvement signaling-mediated confirms regulation helpful maintaining normal function.

Language: Английский

Citations

0

Redox signaling and homeostasis DOI
Xiaoyu Li,

Zichen Cao,

Mo Chen

et al.

Published: April 1, 2025

Language: Английский

Citations

0