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 Table of Contents  
Year : 2018  |  Volume : 13  |  Issue : 11  |  Page : 1879-1882

Cadmium-induced neurotoxicity: still much ado

Department of Experimental and Clinical Medicine, University of Florence, Florence, Italy

Date of Acceptance23-Jul-2018
Date of Web Publication12-Sep-2018

Correspondence Address:
Alessandra Pacini
Department of Experimental and Clinical Medicine, University of Florence, Florence
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/1673-5374.239434

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Cadmium (Cd) is a highly toxic heavy metal that accumulates in living system and as such is currently one of the most important occupational and environmental pollutants. Cd reaches into the environment by anthropogenic mobilization and it is absorbed from tobacco consumption or ingestion of contaminated substances. Its extremely long biological half-life (approximately 20–30 years in humans) and low rate of excretion from the body cause cadmium storage predominantly in soft tissues (primarily, liver and kidneys) with a diversity of toxic effects such as nephrotoxicity, hepatotoxicity, endocrine and reproductive toxicities. Moreover, a Cd-dependent neurotoxicity has been also related to neurodegenerative diseases such as Alzheimer’s and Parkinson’s diseases, amyotrophic lateral sclerosis, and multiple sclerosis. At the cellular level, Cd affects cell proliferation, differentiation, apoptosis and other cellular activities. Among all these mechanisms, the Cd-dependent interference in DNA repair mechanisms as well as the generation of reactive oxygen species, seem to be the most important causes of its cellular toxicity. Nevertheless, there is still much to find out about its mechanisms of action and ways to reduce health risks. This article gives a brief review of the relevant mechanisms that it would be worth investigating in order to deep inside cadmium toxicity.

Keywords: cadmium; toxicity; neurodegenerative disorders; oxidative stress; reactive oxygen species; blood-brain barrier permeability; metallothionein; 17β-estradiol; G-protein-coupled estrogen receptor-30

How to cite this article:
Branca JJ, Morucci G, Pacini A. Cadmium-induced neurotoxicity: still much ado. Neural Regen Res 2018;13:1879-82

How to cite this URL:
Branca JJ, Morucci G, Pacini A. Cadmium-induced neurotoxicity: still much ado. Neural Regen Res [serial online] 2018 [cited 2021 Dec 8];13:1879-82. Available from: http://www.nrronline.org/text.asp?2018/13/11/1879/239434

Cadmium (Cd) is the seventh most toxic heavy metal as per Agency for Toxic Substance and Disease Registry (ATDSR) ranking (Agency for Toxic Substance and Disease Registry, 2017) among the environmental pollutants, widely distributed in natural and industrial sources (reviewed in (Mead, 2010) with which humans and animals can potentially come in contact. Exposure to Cd can occur in occupations as the results of mining and ground water, commercial products, industrial effluents, industrial wastes, vehicle emissions, batteries, fertilizers, paints, and contaminated foods.

Cd can enter the human body by different mechanisms. Cd particles (Cd oxides or Cd dichloride) are transported along primary olfactory neurons and Cd accumulates in the olfactory bulb without further migration into the brain [reviewed in Sunderman (2001)]. Alternatively, after inhalation Cd accumulates into lungs and passing through the alveolar cells gets into the blood circulation [reviewed in Oberdörster (1992)]. Cd uptake by ingestion of Cd-containing food and/or water is the other major mechanism of Cd entry. At the apical membrane of enterocytes Cd is transported by the proton-metal cotransporter divalent metal transporter 1 (DMT1) (also DCT1, Nramp2, or SLC11A2). Cd export through the basolateral membrane is also mediated by transporters such as calcium-ATPases and zinc exporters [reviewed in Bridges and Zalups (2005)].

Following absorption by either lung or the intestinal epithelium, Cd enters the systemic circulation. Blood Cd concentration serves as a biomarker for Cd exposure level and some data indicated that blood Cd concentration in exposed individuals may range from just above 0 μM to 0.05 μM. Nonetheless, the blood Cd concentration of human varies remarkably according to age, gender, diet, residential area, and smoking status (Agency for Toxic Substance and Disease Registry, 2017). The effect of Cd exposure is strictly dose-dependent: at high doses Cd can progressively elicit cell injury, cell death, and organ failure, at low doses it may modulate specific mechanisms without marked cellular toxicity (López et al., 2003; Pacini et al., 2009).

From the outside of cells, Cd can alter the intracellular concentration of calcium which is a universal and versatile intracellular signal messenger (Berridge et al., 2000). Inside cells, Cd regulates Ca2+ signaling by exerting opposite effects on internal Ca2+ pools [Figure 1]a. It blocks the release of stored Ca2+ by inhibiting the activity of 1, 4, 5-trisphosphate (IP3) and ryanodine receptors. In contrast, it increases intracellular Ca2+ concentration by promoting calcium efflux from the sarcoplasmic reticulum [reviewed in Choong et al. (2014)].
Figure 1: Schematic representation of selected cadmium (Cd)-related cellular pathways and nuclear interactions.
AT: Active ATPase transporter; PC: passive channel or carrier; GPCR: G-protein-coupled estrogen receptor-30 (GPR30); G: G-protein; MT: metallothionein; GSH: glutathione; GPx: Glutathione peroxidase; ROS: reactive oxygen species; ER: endoplasmic reticulum.

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Cd can penetrate into neurons via voltage-gated calcium channels (Usai et al., 1999). Indeed, a large body of in vivo and in vitro studies showed that exposure to Cd significantly affects the function of the peripheral (PNS) (Miura et al., 2013) and central nervous system (CNS) [reviewed in Marchetti (2014)] with a wide spectrum of clinical symptoms including olfactory dysfunction, peripheral neuropathy, neurological disturbances, mental retardation, and learning disabilities, as well as motor activity impairment and behavioral alterations both in adults and in children [reviewed in Wang and Du (2013)]. Moreover, Cd-dependent neurotoxicity as been also related to neurodegenerative diseases such as Alzheimer’s (AD) and Parkinson’s diseases (PD) [reviewed in Chin-Chan et al. (2015)], as well as amyotrophic lateral sclerosis and multiple sclerosis [reviewed in Sheykhansari et al. (2018)], and myalgic encephalomyelitis (Pacini et al., 2012).

The uptake of Cd by mammalian cells occurs by both active (ATPase mediated efflux systems and receptor-mediated endocytosis) [Figure 1]b and passive (channels and carriers) transports [Figure 1]c [reviewed in Thévenod (2010)], and the similar chemical properties of Cd2+ and essential metals, especially Ca2+, determine its entry [reviewed in Choong et al. (2014)]. Once inside the cell, the Cd-induced cytotoxicity differs from different organs [reviewed in Rani et al. (2014)], and depends on factors such as its different intracellular distribution (nuclear vs. cytoplasmic). The genotoxicity effect of Cd is known to affect the cell proliferation and differentiation, cell cycle progression, DNA synthesis, and apoptosis. Recently, an important Cd genomic effect is the inhibition of DNA repair [reviewed in Giaginis et al. (2006)] that represents a cause of genomic instability [reviewed in Hartwig et al. (2002)] leading to carcinogenesis, oxidative stress, proto-oncogene activation, altered DNA methylation and dysregulated gene expression [reviewed in Joseph (2009)] [Figure 1]d.

On the other hand, the Cd cytotoxicity depends also on the induction of protective factors among which metallothionein activation, the stimulation of glutathione synthesis, and the presence of antioxidants. This latter feature, in particular, indicates the involvement of reactive oxygen species in the toxic response. Indeed, many reports indicate that the toxic mechanisms of Cd act intracellularly mainly via free-radical-induced production, particularly reactive oxygen species (ROS), which finally culminate into oxidative stress [reviewed in Jomova and Valko (2011)]. Many data regarding the modifications in thiol groups of antioxidant enzymes induced by oxidative stress are reported [extensively reviewed in Yang and Lee (2015)]. However, damage caused by low levels of oxidative stress can be neutralized by anti-oxidant enzymes. After exposure to low-dose Cd (1–10 μM), expression and activity of antioxidant enzymes including metallothionein (MT), catalase, glutathione S-transferase, glutathione peroxidase, and quinone oxidoreductase were substantially increased as well as the glutathione (GSH) cellular levels [extensively reviewed in Sandbichler and Höckner (2016)]. On the other hand, since Cd has a high affinity to thiol groups, proteins containing thiol groups including MT and GSH are major carriers of Cd [Figure 1]e.

Many studies have demonstrated that essential metals dietary supplements play important roles in protecting against Cd. Possessing similar chemical and physical properties to Cd, zinc (Zn) competes for binding sites of enzymatic proteins and induces the synthesis of the CNS specific metallothionein III that, in turn, binds to Cd causing its detoxification [Figure 1]f. Moreover, Zn alleviates the Cd-dependent oxidative stress [reviewed in Matović et al. (2011)]. In addition to Zn, also selenium (Se) has been demonstrated to protect against Cd neurotoxicity. Indeed, as an important cofactor of the selenium glutathione peroxidase (GPx) enzyme [Figure 1]g, on the one hand reduces oxidative stress, on the other enhances the cellular antioxidant capacity [reviewed in Nemmiche (2017)]. Despite the proven protective effects of Se against Cd neurotoxicity, it is important to highlight that the efficacy of Se strictly depends on the neuronal subtype. Recently, we have demonstrated that whereas Se is effective on catecholaminergic neurons, it is ineffective on cholinergic neurons (Branca et al., 2018). To this end, it is also important to stress that some subsets of cholinergic neurons express low levels of GPx (Trépanier et al., 1996); thus it is plausible to hypothesize that the lack of Se-mediated protection against Cd neurotoxicity in cholinergic neurons might be linked to their intrinsic GPx deficiency. The notion that the effects of Cd on the brain is region-specific (Kumar et al., 1996) would lend support to this hypothesis. To this regard, however, one of the key question that needs addressing is to understand the reason for the differential expression of the GPx enzyme in some subsets of cholinergic neurons (Trépanier et al., 1996).

Another interesting aspect that needs further investigation is the lack of ability of the Cd to penetrate the adult blood-brain barrier (BBB) and the blood-spinal fluid barrier, as well as the ependymal and pial surface. As a consequence young subjects that lack a fully operational BBB are more vulnerable to Cd (Antonio et al., 2002). However, even if many experimental studies have shown extensive histopathological damage in the cerebral and cerebellar cortices of growing animals compared to the adults, the mechanism concerning transport and metabolism of Cd in the brain is very poor. Furthermore, as mentioned above, Cd has been linked to the onset of several neurodegenerative diseases, such as AD, PD, and chronic traumatic encephalopathy characterized by alterations of the BBB (Shukla and Chandra, 1987; Shukla et al., 1987). This notion makes it plausible to hypothesize that Cd-mediated alterations of the BBB are at the basis of the degenerative disorders. This hypothesis is also supported by the observation of in vivo BBB dysfunction by exposure to Cd (Shukla et al., 1996).

To this end it would be important to dissect in details the molecular mechanism underlying Cd-dependent BBB alteration, and to determine whether the vascular endothelial cells lining the luminal surface of blood brain vessels are the primary potential target of circulating Cd, which might be important to explain the BBB alterations. This approach would help to ascertain whether BBB alterations could be primarily responsible for the effects of Cd on the CNS.

On the other hand, it would be important to address the role of the choroidal epithelia as the first line of defense against the detrimental effects of Cd on the CNS. The choroidal plexus, containing abundant metal binding ligands as well as high cystine concentration and significantly higher activities of superoxide dismutase and catalase, may effectively sequester Cd and prevent Cd entry into the CNS [reviewed in Zheng (2001)]. Thus, the need arises for a more comprehensive understanding of the molecular mechanisms that operate also in the choroid cells.

Another important aspect that has received little attention, is the estrogen-like effect of Cd. Cd is a well-known xenoestrogen that binds to estrogen receptor alpha and blocks the binding of 17β-estradiol in a noncompetitive manner. However, there is increasing evidence that G-protein-coupled estrogen receptor-30 (GPR30), a novel estrogen receptor, can mediate many estrogenic effects on the vasculature. GPR30 is a seven-transmembrane-spanning receptor that specifically binds to 17β-estradiol and causes rapid intracellular signaling. GPR30 has been linked to specific estrogen binding and rapid signaling [reviewed in Barton et al. (2018)]. Several groups have demonstrated GPR30 expression in the vascular endothelium of rodents and human cells evidencing an induction of actin polymerization and arrangement, as well as an inhibition of proliferation by the GPR30 selective agonist G-1 (Rowlands et al., 2011). Moreover, GPR30 has been demonstrated to mediate the proliferation of breast cancer cells induced by Cd (Yu et al., 2010). Nevertheless, the functional significance of this endothelial GPR30 is still largely unknown. A more extensive evaluation of GPR30 expression in barrier endothelial cells and the role of Cd in their stimulation and/or inhibition could open new scenarios in the understanding of the neurotoxic effects of Cd [Figure 1]h.

The complexity of Cd-dependent neurotoxicity and its multiple effects in neural tissue points to its toxicity on brain homeostasis.[36]

In conclusion, many aspects of the molecular mechanisms ensuing the entry of Cd into the cell remain to be clarified and more in vivo and in vitro studies are needed to thoroughly elucidate Cd-dependent relevant signaling cascades.

Author contributions: JJVB collected data and wrote the manuscript, GM participated discussion and provide suggestion, AP provided opinion and revised manuscript.

Conflicts of interest: There are no conflicts of interest associated with this manuscript.

Financial support: None.

Copyright license agreement: The Copyright License Agreement has been signed by all authors before publication.

Plagiarism check: Checked twice by iThenticate.

Peer review: Externally peer reviewed.

Open peer reviewer: Colin Barnstable, Pennsylvania State University College of Medicine, USA.

Additional file: Open peer review report 1.[Additional file 1]

  References Top

Agency for Toxic Substance and Disease Registry USA (2017) Toxicological Profile for Cadmium. Department of Health and Humans Services, Public Health Service, Centers for Disease Control, Atlanta, GA, USA.  Back to cited text no. 1
Antonio MT, López N, Leret ML (2002) Pb and Cd poisoning during development alters cerebellar and striatal function in rats. Toxicology 176:59-66.  Back to cited text no. 2
Barton M, Filardo EJ, Lolait SJ, Thomas P, Maggiolini M, Prossnitz ER (2018) Twenty years of the G protein-coupled estrogen receptor GPER: Historical and personal perspectives. J Steroid Biochem Mol Biol 176:4-15.  Back to cited text no. 3
Berridge MJ, Lipp P, Bootman MD (2000) The versatility and universality of calcium signalling. Nat Rev Mol Cell Biol 1:11-21.  Back to cited text no. 4
Branca JJV, Morucci G, Maresca M, Tenci B, Cascella R, Paternostro F, Ghelardini C, Gulisano M, Di Cesare Mannelli L, Pacini A (2018) Selenium and zinc: Two key players against cadmium-induced neuronal toxicity. Toxicol In Vitro 48:159-169.  Back to cited text no. 5
Bridges CC, Zalups RK (2005) Molecular and ionic mimicry and the transport of toxic metals. Toxicol Appl Pharmacol 204:274-308.  Back to cited text no. 6
Chin-Chan M, Navarro-Yepes J, Quintanilla-Vega B (2015) Environmental pollutants as risk factors for neurodegenerative disorders: Alzheimer and Parkinson diseases. Front Cell Neurosci 9:124.  Back to cited text no. 7
Choong G, Liu Y, Templeton DM (2014) Interplay of calcium and cadmium in mediating cadmium toxicity. Chem Biol Interact 211:54-65.  Back to cited text no. 8
Giaginis C, Gatzidou E, Theocharis S (2006) DNA repair systems as targets of cadmium toxicity. Toxicol Appl Pharmacol 213:282-290.  Back to cited text no. 9
Hartwig A, Asmuss M, Blessing H, Hoffmann S, Jahnke G, Khandelwal S, Pelzer A, Burkle A (2002) Interference by toxic metal ions with zinc-dependent proteins involved in maintaining genomic stability. Food Chem Toxicol 40:1179-1184.  Back to cited text no. 10
Jomova K, Valko M (2011) Advances in metal-induced oxidative stress and human disease. Toxicology 283:65-87.  Back to cited text no. 11
Joseph P (2009) Mechanisms of cadmium carcinogenesis. Toxicol Appl Pharmacol 238:272-279.  Back to cited text no. 12
Kumar R, Agarwal AK, Seth PK (1996) Oxidative stress-mediated neurotoxicity of cadmium. Toxicol Lett 89:65-69.  Back to cited text no. 13
López E, Figueroa S, Oset-Gasque MJ, González MP (2003) Apoptosis and necrosis: two distinct events induced by cadmium in cortical neurons in culture. Br J Pharmacol 138:901-911.  Back to cited text no. 14
Marchetti C (2014) Interaction of metal ions with neurotransmitter receptors and potential role in neurodiseases. Biometals 27:1097-1113.  Back to cited text no. 15
Matović V, Buha A, Bulat Z, Dukić-Ćosić D (2011) Cadmium toxicity revisited: focus on oxidative stress induction and interactions with zinc and magnesium. Arh Hig Rada Toksikol 62:65-76.  Back to cited text no. 16
Mead MN (2010) Cadmium confusion: do consumers need protection? Environ Health Perspect 118:a528-534.  Back to cited text no. 17
Miura S, Takahashi K, Imagawa T, Uchida K, Saito S, Tominaga M, Ohta T (2013) Involvement of TRPA1 activation in acute pain induced by cadmium in mice. Mol Pain 9:7.  Back to cited text no. 18
Nemmiche S (2017) Oxidative signaling response to cadmium exposure. Toxicol Sci 156:4-10.  Back to cited text no. 19
Oberdörster G (1992) Pulmonary deposition, clearance and effects of inhaled soluble and insoluble cadmium compounds. IARC Sci Publ:189-204.  Back to cited text no. 20
Pacini S, Punzi T, Morucci G, Gulisano M, Ruggiero M (2009) A paradox of cadmium: a carcinogen that impairs the capability of human breast cancer cells to induce angiogenesis. J Environ Pathol Toxicol Oncol 28:85-88.  Back to cited text no. 21
Rani A, Kumar A, Lal A, Pant M (2014) Cellular mechanisms of cadmium-induced toxicity: a review. Int J Environ Health Res 24:378-399.  Back to cited text no. 22
Rowlands DJ, Chapple S, Siow RC, Mann GE (2011) Equol-stimulated mitochondrial reactive oxygen species activate endothelial nitric oxide synthase and redox signaling in endothelial cells: roles for F-actin and GPR30. Hypertension 57:833-840.  Back to cited text no. 23
Sandbichler AM, Höckner M (2016) Cadmium protection strategies--a hidden trade-off? Int J Mol Sci 17:E139.  Back to cited text no. 24
Sheykhansari S, Kozielski K, Bill J, Sitti M, Gemmati D, Zamboni P, Singh AV (2018) Redox metals homeostasis in multiple sclerosis and amyotrophic lateral sclerosis: a review. Cell Death Dis 9:348.  Back to cited text no. 25
Shukla A, Shukla GS, Srimal RC (1996) Cadmium-induced alterations in blood-brain barrier permeability and its possible correlation with decreased microvessel antioxidant potential in rat. Hum Exp Toxicol 15:400-405.  Back to cited text no. 26
Shukla GS, Chandra SV (1987) Concurrent exposure to lead, manganese, and cadmium and their distribution to various brain regions, liver, kidney, and testis of growing rats. Arch Environ Contam Toxicol 16:303-310.  Back to cited text no. 27
Shukla GS, Hussain T, Chandra SV (1987) Possible role of regional superoxide dismutase activity and lipid peroxide levels in cadmium neurotoxicity: in vivo and in vitro studies in growing rats. Life Sci 41:2215-2221.  Back to cited text no. 28
Sunderman FW Jr (2001) Nasal toxicity, carcinogenicity, and olfactory uptake of metals. Ann Clin Lab Sci 31:3-24.  Back to cited text no. 29
Thévenod F (2010) Catch me if you can! Novel aspects of cadmium transport in mammalian cells. Biometals 23:857-875.  Back to cited text no. 30
Trépanier G, Furling D, Puymirat J, Mirault ME (1996) Immunocytochemical localization of seleno-glutathione peroxidase in the adult mouse brain. Neuroscience 75:231-243.  Back to cited text no. 31
Usai C, Barberis A, Moccagatta L, Marchetti C (1999) Pathways of cadmium influx in mammalian neurons. J Neurochem 72:2154-2161.  Back to cited text no. 32
Wang B, Du Y (2013) Cadmium and its neurotoxic effects. Oxid Med Cell Longev 2013:898034.  Back to cited text no. 33
Yang HY, Lee TH (2015) Antioxidant enzymes as redox-based biomarkers: a brief review. BMB Reports 48:200-208.  Back to cited text no. 34
Yu X, Filardo EJ, Shaikh ZA (2010) The membrane estrogen receptor GPR30 mediates cadmium-induced proliferation of breast cancer cells. Toxicol Appl Pharmacol 245:83-90.  Back to cited text no. 35
Zheng W (2001) Toxicology of choroid plexus: special reference to metal-induced neurotoxicities. Microsc Res Tech 52:89-103.  Back to cited text no. 36


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[Pubmed] | [DOI]
M. M. Ziatdinova,T. G. Yakupova,Ya. V. Valova,G. F. Mukhammadieva,D. O. Karimov,L. Sh. Nazarova,D. A. Smolyankin
Toxicological Review. 2021; (6): 38
[Pubmed] | [DOI]
33 Synaptic mechanisms of cadmium neurotoxicity
AndreiN Tsentsevitsky,AlexeyM Petrov
Neural Regeneration Research. 2021; 16(9): 1762
[Pubmed] | [DOI]
34 Egg white hydrolysate prevents reproductive impairments induced by cadmium in rats
José Eudes Gomes Pinheiro,Caroline Silveira Martinez,Paola Zambelli Moraes,José Eduardo Stasiaki,Maria Elisa Trost,Dalton Valentim Vassallo,Fernando Barbosa,Franck Maciel Peçanha,Francielli Weber Santos Cibin,Marta Miguel,Giulia Alessandra Wiggers
Journal of Functional Foods. 2020; 67: 103823
[Pubmed] | [DOI]
35 Redox and essential metal status in the brain of Wistar rats acutely exposed to a cadmium and lead mixture
Dragana Javorac,Aleksandra Buha Đordevic,Milena Andelkovic,Simona Tatovic,Katarina Baralic,Evica Antonijevic,Jelena Kotur-Stevuljevic,Danijela Đukic-Cosic,Biljana Antonijevic,Zorica Bulat
Archives of Industrial Hygiene and Toxicology. 2020; 71(3): 197
[Pubmed] | [DOI]
36 Egg case concentrate of Mantis religiosa abrogates the accumulation of cadmium in muscular and bone tissues of African catfish via activation of nitric oxide and myeloperoxidase activity
J. K. Akintunde,I. A. Imhade,G. Oboh
Journal of Food Biochemistry. 2020;
[Pubmed] | [DOI]
37 Wnt pathway: A mechanism worth considering in endocrine disrupting chemical action
Ünsal Veli Üstündag,Ebru Emekli-Alturfan
Toxicology and Industrial Health. 2020; 36(1): 41
[Pubmed] | [DOI]
38 Selenium modifies associations between multiple metals and neurologic symptoms in Gulf states residents
Emily J. Werder,Lawrence S. Engel,Matthew D. Curry,Dale P. Sandler
Environmental Epidemiology. 2020; 4(6): e115
[Pubmed] | [DOI]
39 Hazard identification, classification, and risk assessment of carcinogens: too much or too little? – Report of an ECETOC workshop
Susan P. Felter,Alan R. Boobis,Philip A. Botham,Alice Brousse,Helmut Greim,Heli M. Hollnagel,Ursula G. Sauer
Critical Reviews in Toxicology. 2020; 50(1): 72
[Pubmed] | [DOI]
40 Attenuation of cadmium-induced vascular toxicity by pro-angiogenic nanorods
Arpita Roy,Susheel Kumar Nethi,Natarajan Suganya,Megha Raval,Suvro Chatterjee,Chitta Ranjan Patra
Materials Science and Engineering: C. 2020; : 111108
[Pubmed] | [DOI]
41 Disruption of essential metal homeostasis in the brain by cadmium and high-fat diet
John C. Mazzocco,Rekha Jagadapillai,Evelyne Gozal,Maiying Kong,Qian Xu,Gregory N. Barnes,Jonathan H. Freedman
Toxicology Reports. 2020; 7: 1164
[Pubmed] | [DOI]
42 Exposure to Aluminum, Cadmium, and Mercury and Autism Spectrum Disorder in Children: A Systematic Review and Meta-Analysis
Rosalind Sulaiman,Meng Wang,Xuefeng Ren
Chemical Research in Toxicology. 2020;
[Pubmed] | [DOI]
43 Histological changes, lipid metabolism, and oxidative and endoplasmic reticulum stress in the liver of laying hens exposed to cadmium concentrations
M.K. Zhu,H.Y. Li,L.H. Bai,L.S. Wang,X.T. Zou
Poultry Science. 2020;
[Pubmed] | [DOI]
44 Protocatechuic acid mitigates cadmium-induced neurotoxicity in rats: Role of oxidative stress, inflammation and apoptosis
Ebtesam M. Al Olayan,Abeer S. Aloufi,Ohoud D. AlAmri,Ola H. El-Habit,Ahmed E. Abdel Moneim
Science of The Total Environment. 2020; 723: 137969
[Pubmed] | [DOI]
45 Morphine-element interactions – The influence of selected chemical elements on neural pathways associated with addiction
Patrycja Kupnicka,Klaudyna Kojder,Emilia Metryka,Patrycja Kapczuk,Dariusz Jezewski,Izabela Gutowska,Marta Goschorska,Dariusz Chlubek,Irena Baranowska-Bosiacka
Journal of Trace Elements in Medicine and Biology. 2020; 60: 126495
[Pubmed] | [DOI]
46 Cadmium desynchronizes neurotransmitter release in the neuromuscular junction: Key role of ROS
A.N. Tsentsevitsky,G.F. Zakyrjanova,A.M. Petrov
Free Radical Biology and Medicine. 2020;
[Pubmed] | [DOI]
47 A novel macrocycle acridine-based fluorescent chemosensor for selective detection of Cd2+ in Brazilian sugarcane spirit and tobacco cigarette smoke extract
Fabiane dos Santos Carlos,Letícia Aparecida da Silva,Cristiano Zanlorenzi,Fábio Souza Nunes
Inorganica Chimica Acta. 2020; 508: 119634
[Pubmed] | [DOI]
48 Single-cell RNA Sequencing of Mouse Neural Stem Cell Differentiation Reveals Adverse Effects of Cadmium on Neurogenesis
Bo Song,Guiya Xiong,Huan Luo,Zhenzi Zuo,Zhijun Zhou,Xiuli Chang
Food and Chemical Toxicology. 2020; : 111936
[Pubmed] | [DOI]
49 First evidence of the protective role of melatonin in counteracting cadmium toxicity in the rat ovary via the mTOR pathway
Safa Kechiche,Massimo Venditti,Latifa Knani,Karolina Jablonska,Piotr Dziegiel,Imed Messaoudi,Russel J. Reiter,Sergio Minucci
Environmental Pollution. 2020; : 116056
[Pubmed] | [DOI]
50 Development of a Drosophila melanogaster based model for the assessment of cadmium and mercury mediated renal tubular toxicity
Sanjay Saini,Lavi Rani,Neha Shukla,Monisha Banerjee,Debapratim Kar Chowdhuri,Naveen Kumar Gautam
Ecotoxicology and Environmental Safety. 2020; 201: 110811
[Pubmed] | [DOI]
51 Cadmium exposure negatively affects the microarchitecture of trabecular bone and decreases the density of a subset of sympathetic nerve fibers innervating the developing rat femur
Mayra A. Graniel-Amador,Héctor F. Torres-Rodríguez,Juan M. Jiménez-Andrade,Joel Hernández-Rodríguez,Marcela Arteaga-Silva,Sergio Montes
BioMetals. 2020;
[Pubmed] | [DOI]
52 Involvement of the synapse-specific zinc transporter ZnT3 in cadmium-induced hippocampal neurotoxicity
Safa Ben Mimouna,Tifenn Le Charpentier,Sophie Lebon,Juliette Van Steenwinckel,Imed Messaoudi,Pierre Gressens
Journal of Cellular Physiology. 2019;
[Pubmed] | [DOI]
53 Toxicant-mediated redox control of proteostasis in neurodegeneration
Stefanos Aivazidis,Colin C. Anderson,James R. Roede
Current Opinion in Toxicology. 2019; 13: 22
[Pubmed] | [DOI]
54 Back to Nucleus: Combating with Cadmium Toxicity Using Nrf2 Signaling Pathway as a Promising Therapeutic Target
Milad Ashrafizadeh,Zahra Ahmadi,Tahereh Farkhondeh,Saeed Samarghandian
Biological Trace Element Research. 2019;
[Pubmed] | [DOI]
55 Association of Acute, High-dose Cadmium Exposure with Alterations in Vascular Endothelial Barrier Antigen Expression and Astrocyte Morphology in the Developing Rat Central Nervous System
M.O. Ibiwoye,Q. Matthews,K. Travers,J.D. Foster
Journal of Comparative Pathology. 2019; 172: 37
[Pubmed] | [DOI]
56 A fluorogenic probe based on chelation–hydrolysis-enhancement mechanism for visualizing Zn2+ in Parkinsonćs disease models
Gaobin Zhang,Yanfei Zhao,Bo Peng,Zheng Li,Chenchen Xu,Yi Liu,Chengwu Zhang,Nicolas H. Voelcker,Lin Li,Wei Huang
Journal of Materials Chemistry B. 2019;
[Pubmed] | [DOI]
57 Cardiotoxicity of Intravenously Administered CdSe/ZnS Quantum Dots in BALB/c Mice
Li Li,Jinglin Tian,Xiaomei Wang,Gaixia Xu,Wenxiao Jiang,Zhiwen Yang,Dongmeng Liu,Guimiao Lin
Frontiers in Pharmacology. 2019; 10
[Pubmed] | [DOI]
58 The effects of quercetin on antioxidant and cytokine levels in rat hippocampus exposed to acute cadmium toxicity
Ihsan KISADERE,Nurcan DÖNMEZ,Hasan Hüseyin DÖNMEZ
Journal of Cellular Neuroscience and Oxidative Stress. 2019; 11(2): 10
[Pubmed] | [DOI]
59 Application of metabolomics to characterize environmental pollutant toxicity and disease risks
Pan Deng,Xusheng Li,Michael C. Petriello,Chunyan Wang,Andrew J. Morris,Bernhard Hennig
Reviews on Environmental Health. 2019; 34(3): 251
[Pubmed] | [DOI]
60 Cannabidiol Protects Dopaminergic Neuronal Cells from Cadmium
Jacopo Junio Valerio Branca,Gabriele Morucci,Matteo Becatti,Donatello Carrino,Carla Ghelardini,Massimo Gulisano,Lorenzo Di Cesare Mannelli,Alessandra Pacini
International Journal of Environmental Research and Public Health. 2019; 16(22): 4420
[Pubmed] | [DOI]
61 EDTA Chelation Therapy for the Treatment of Neurotoxicity
Fulgenzi Alessandro,Ferrero Maria Elena
International Journal of Molecular Sciences. 2019; 20(5): 1019
[Pubmed] | [DOI]
62 Effects of Cadmium on ZO-1 Tight Junction Integrity of the Blood Brain Barrier
Jacopo Junio Valerio Branca,Mario Maresca,Gabriele Morucci,Tommaso Mello,Matteo Becatti,Luigia Pazzagli,Ilaria Colzi,Cristina Gonnelli,Donatello Carrino,Ferdinando Paternostro,Claudio Nicoletti,Carla Ghelardini,Massimo Gulisano,Lorenzo Di Cesare Mannelli,Alessandra Pacini
International Journal of Molecular Sciences. 2019; 20(23): 6010
[Pubmed] | [DOI]


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