Research progress on metal pollutants inducing neurotoxicity through ferroptosis DOI
Zhiqiang Qin, Yuqing Chen, Xinyuan Zhao

et al.

Journal of Zhejiang University (Medical Sciences), Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 1, 2024

It has been confirmed that exposure to various metal pollutants can induce neurotoxicity, which is closely associated with the occurrence and development of neurological disorders. Ferroptosis a form cell death in response pollutant it related oxidative stress, iron metabolism lipid peroxidation. Recent studies have revealed ferroptosis plays significant role neurotoxicity induced by metals such as lead, cadmium, manganese, nickel, antimony. Lead triggers through disorder inflammation. Cadmium ion metabolism, stress signaling pathways IRE1/JNK/FTH1. Manganese promote mitochondrial dysfunction, stress. Nickel influencing function, disrupting homeostasis facilitating peroxidation central nervous system. Antimony glutathione depletion activating autophagy, resulting excessive intracellular deposition ultimately causing ferroptosis. This article reviews effects on ferroptosis-related indicators discusses specific mechanisms each may provide references identify targets preventing develop treatment strategies

Language: Английский

Ferroptosis Induced by Pollutants: An Emerging Mechanism in Environmental Toxicology DOI

Lili Yang,

Xiaoming Cai,

Ruibin Li

et al.

Environmental Science & Technology, Journal Year: 2024, Volume and Issue: 58(5), P. 2166 - 2184

Published: Jan. 26, 2024

Environmental pollutants have been recognized for their ability to induce various adverse outcomes in both the environment and human health, including inflammation, apoptosis, necrosis, pyroptosis, autophagy. Understanding these biological mechanisms has played a crucial role risk assessment management efforts. However, recent identification of ferroptosis as form programmed cell death emerged critical mechanism underlying pollutant-induced toxicity. Numerous studies demonstrated that fine particulates, heavy metals, organic substances can trigger ferroptosis, which is closely intertwined with lipid, iron, amino acid metabolism. Given growing evidence linking severe diseases such heart failure, chronic obstructive pulmonary disease, liver injury, Parkinson's Alzheimer's cancer, it imperative investigate ferroptosis. In this review, we comprehensively analyze pathways intricate signaling molecules elucidate integration into driving braking axes. Furthermore, discuss potential hazards associated organs four representative animal models. Finally, provide an outlook on future research directions strategies aimed at preventing By enhancing our understanding novel developing effective preventive measures, mitigate effects environmental safeguard health.

Language: Английский

Citations

38
The interplay of transition metals in ferroptosis and pyroptosis DOI Creative Commons

Frantisek Vana,

Zoltán Szabó, Michal Masařík

et al.

Cell Division, Journal Year: 2024, Volume and Issue: 19(1)

Published: Aug. 3, 2024

Cell death is one of the most important mechanisms maintaining homeostasis in our body. Ferroptosis and pyroptosis are forms necrosis-like cell death. These modalities play key roles pathophysiology cancer, cardiovascular, neurological diseases, other pathologies. Transition metals abundant group elements all living organisms. This paper presents a summary ferroptosis pathways their connection to significant transition metals, namely zinc (Zn), copper (Cu), molybdenum (Mo), lead (Pb), cobalt (Co), iron (Fe), cadmium (Cd), nickel (Ni), mercury (Hg), uranium (U), platinum (Pt), crucial element, selenium (Se). Authors aim summarize up-to-date knowledge this topic.In review, there categorized highlighted common patterns alterations by metals. Special attention given since collected data support its dual nature action both pyroptosis. All findings presented together with brief description major biochemical involving mentioned visualized attached comprehensive figures.This work concludes that majority disruptions studied metals' impacts fate, influencing survival cells complex system altered pathways. Therefore, opens up space for further research.

Language: Английский

Citations

8
Selenium nanoparticles alleviates cadmium induced hepatotoxicity by inhibiting ferroptosis and oxidative stress in vivo and in vitro DOI

Chunyan Shao,

Tongwang Luo, Shujie Wang

et al.

Chemosphere, Journal Year: 2024, Volume and Issue: 364, P. 143004 - 143004

Published: Aug. 3, 2024

Language: Английский

Citations

7
Molybdenum and cadmium co-induce apoptosis and ferroptosis through inhibiting Nrf2 signaling pathway in duck (Anas platyrhyncha) testes DOI Creative Commons
Jiamei Zhu, Xueyan Dai, Yán Wāng

et al.

Poultry Science, Journal Year: 2024, Volume and Issue: 103(5), P. 103653 - 103653

Published: March 13, 2024

Cadmium (Cd) and high molybdenum (Mo) are injurious to the body. Previous research has substantiated that Cd Mo exposure caused testicular injury of ducks, but concrete mechanism is not fully clarified. To further survey toxicity co-exposure in testis, 40 healthy 8-day-old Shaoxing ducks (Anas platyrhyncha) were stochasticly distributed four groups raised with basic diet embracing (4 mg/kg Cd) or (100 Mo) both. At 16th week, testis tissues gathered. The characteristic ultrastructural changes related apoptosis ferroptosis observed both groups. Besides, repressed nuclear factor erythroid 2-related 2(Nrf2) pathway via decreasing Nrf2, Heme oxygenase-1 (HO-1), NAD(P)H quinone oxidoreductase 1 (NQO1), Glutamate-cysteine ligase catalytic subunit (GCLC) modifier (GCLM) mRNA expression Nrf2 protein expression, then stimulated by elevating Bcl-2 antagonist/killer-1 (Bak-1), Bcl-2-associated X-protein (Bax), Cytochrome complex (Cyt-C), caspase-3 cleaved-caspase-3 rate, as well reducing B-cell lymphoma-2 (Bcl-2) ratio Bax, triggered upregulating Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4), transferrin receptor (TFR1) Prostaglandin-Endoperoxide Synthase 2 (PTGS2) levels, downregulating ferritin heavy chain (FTH1), light (FTL1), ferroportin (FPN1), solute carrier family 7 member 11 (SCL7A11) glutathione peroxidase (GPX4) levels. most obvious these indexes co-treated group. Altogether, results announced evoked inhibiting exacerbated variations.

Language: Английский

Citations

5
Exosomes drive ferroptosis by stimulating iron accumulation to inhibit bacterial infection in crustaceans DOI Creative Commons
Qian Sun,

Jiawen Yang,

Ming Zhang

et al.

Journal of Biological Chemistry, Journal Year: 2023, Volume and Issue: 299(12), P. 105463 - 105463

Published: Nov. 15, 2023

Ferroptosis, characterized by iron-dependent cell death, has recently emerged as a critical defense mechanism against microbial infections. The present study aims to investigate the involvement of exosomes in induction ferroptosis and inhibition bacterial infection crustaceans. Our findings provide compelling evidence for pivotal role immune response crustaceans, wherein they facilitate intracellular iron accumulation activate ferroptotic pathways. Using RNA-seq bioinformatic analysis, we demonstrate that cytochrome P450 (CYP) can effectively trigger ferroptosis. Moreover, conducting an analysis exosome cargo proteins, have identified participation six-transmembrane epithelial antigen prostate 4 regulation hemocyte sensitivity. Subsequent functional investigations unveil enhances cellular Fe

Language: Английский

Citations

13
A Drosophila model of gestational antimony exposure uncovers growth and developmental disorders caused by disrupting oxidative stress homeostasis DOI
Xiaoke Wang,

Peiyao Zhou,

Ziyang Zhang

et al.

Free Radical Biology and Medicine, Journal Year: 2023, Volume and Issue: 208, P. 418 - 429

Published: Sept. 2, 2023

Language: Английский

Citations

11
ATF3 as a response factor to regulate Cd-induced reproductive damage by activating the NRF2/HO-1 ferroptosis pathway DOI Creative Commons
Sisi Li, Sheng Ma, Lirui Wang

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2024, Volume and Issue: 285, P. 117114 - 117114

Published: Oct. 1, 2024

Language: Английский

Citations

4
Toxicity of antimony in housefly after whole-life-cycle exposure: Changes in growth, development, redox homeostasis, mitochondrial function, and fecundity DOI Creative Commons
Yuming Zhang,

Jinghua Lv,

Xiaoli Sun

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2025, Volume and Issue: 289, P. 117656 - 117656

Published: Jan. 1, 2025

The increasing utilization of antimony (Sb) in manufacturing industries has led to the emergence Sb contamination environment as a significant public health concern. To elucidate toxicity and its mechanism action, this study aimed investigate adverse effects on cosmopolitan insect, housefly (Musca domestica), under whole life cycle (from embryonic adult stage) exposure through examination suite parameters, including biological, physiological, behavioral, molecular endpoints. A range concentrations, moderate (0.07 mM), heavy (0.7 extreme (7 70 were conducted study. results indicated that houseflies could maintain their when exposed 0.07 mM Sb. (0.7-70 mM) resulted effects, developmental retardation, locomotor inhibition, gut damage, oxidative stress, mitochondrial dysfunction houseflies. Significantly, demonstrated reproductive houseflies, evidenced by reduced capacity, DNA ovarian abnormalities. disturbance hormonal synthesis MAPK pathway induced treatment may contribute toxicity. These comprehensive toxicological data provide insight into prediction assessment ecological risk

Language: Английский

Citations

0
Molecular insight into reproductive toxicity and transgenerational effects of Cadmium exposure on Drosophila melanogaster DOI Creative Commons
Yi Pan,

Ke Fan,

Linhao Zong

et al.

Ecotoxicology and Environmental Safety, Journal Year: 2025, Volume and Issue: 291, P. 117870 - 117870

Published: Feb. 1, 2025

Cadmium (Cd), a widespread and serious environmental pollutant, has recently garnered increasing scientific scrutiny due to its profound adverse effects. Although the evidence for Cd-induced reproductive toxicity is well established, it remains elusive on intricate dose-response relationship underlying molecular mechanisms, especially transgenerational in animals. Here, we employed fruit fly (Drosophila melanogaster) as model organism examine performance across five generations by parental exposure varying concentrations of Cd (5, 50, 500 μM). Firstly, our observations number eggs laid, pupae formed, adult flies emerged directly exposed generation (F0) confirmed dose-dependent decline fecundity. Transcriptome analysis revealed that, oxidative stress ion transport disruption F0 could underlie synaptic dysfunction impaired follicle cell development, impacting behavior oocyte fertility. Employing analysis, Wnt signaling pathway mTOR were identified early responses toxicity. Secondly, sustained detrimental effects observed at least two three after removal. At epigenetic level, perturb fecundity modulating Dnmt2 expression, pivotal regulator methylation processes. Moreover, despite phenotypic recovery F4, persistent changes indicate enduring toxicity, highlighting need vigilance against contamination long-term Collectively, findings enhance understanding effects, highlight further improve assessment multigenerational consequences contamination.

Language: Английский

Citations

0
Ferritin1-mediated ferroptosis participates in granular acini degeneration of Haemaphysalis longicornis salivary glands DOI Creative Commons
Dongqi Yuan,

Songqin Chen,

Yongzhi Zhou

et al.

Ticks and Tick-borne Diseases, Journal Year: 2025, Volume and Issue: 16(2), P. 102464 - 102464

Published: March 1, 2025

Ticks (Haemaphysalis longicornis) transmit pathogens to their hosts through salivary glands during blood-feeding. The of adult parthenogenetic H. longicornis undergo degeneration post-engorgement. Clarifying the molecular mechanisms underlying gland is conducive identifying novel targets for preventing and controlling these widespread vectors. In this study, we investigated elucidate relationship between ferroptosis, iron-dependent cell death, ferritin 1 (HlFer1) post-attachment Fluorescence microscopy, revealed increased iron accumulation, reactive oxygen species, lipid peroxidation, decreased mitochondrial cristae in granular acini results a qPCR analysis indicated that HlFer1, glutathione peroxidase 4 (GPX4), transferrin (TRF), high mobility group protein B1 (HMGB1) expression elevated vitro culture showed erastin promotes while ferrostatin-1 blocks process. RNA interference (RNAi) targeting HlFer1 promoted ferroptosis acini. conclusion, demonstrated HlFer1-induced key mechanism longicornis. Our findings are important developing preventive measures against as disease vector.

Language: Английский

Citations

0