Microstructure and Ultrastructure Alterations in the Pallium of Immature Mice Exposed to Cadmium

Yang, X. F.; Han, Qing; Liu, D. Y.; Zhang, H. T.; Fan, G. Y.; Y., J.; Wang, Z. L.

doi:10.1007/s12011-016-0657-8

Cited by 6 publications

(3 citation statements)

References 26 publications

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“…xenobiotic in the case of the administration in our study of the diet containing 5 mg Cd/kg, which corresponded to the moderate exposure of the general population to this xenobiotic, reached 0.405 mg Cd/kg bw or 0.660 mg CdCl 2 /kg bw(Brz oska et al, 2015). The same refers to the exposure to 3.74 or 7.84 mg CdCl 2 /kg bw for 40 days in the study byYang et al (2016) that Changes in the behaviour, motor activity and memory function of experimental animals due to exposure to Cd The impact of exposure to Cd on the oxidative-reductive status of the brain tissue of experimental animals…”

supporting

confidence: 68%

“…Structural abnormalities in the different parts of the brain including the cerebral cortex, cerebellum, pallium and hippocampus were observed in the experimental animals after short‐ and long‐lasting exposure to various doses or concentrations of this heavy metal (Tables 2 and 3 ) (Ibiwoye et al, 2019 ; PM et al, 2019 ; Pulido et al, 2019 ; Yang et al, 2015 , 2016 ). Numerous studies in animal models have revealed that short‐ and long‐term intoxication with different doses of Cd decreases locomotor activity, as well as causes memory dysfunction, raised anxiety, aggressiveness and disturbances of sleep (Table 4 ) (Chouit et al, 2021 ; Haider et al, 2015 ; Pan et al, 2017 ; Pulido et al, 2019 ; Terçariol et al, 2011 ; Unno et al, 2014 ; Wang, Zhang, et al, 2018 ; Yang et al, 2015 , 2016 ). It is worth underlining that exposure to Cd of adult animals can result in occurring neurotoxic effects in their offspring (Tian et al, 2020 ; Zhao et al, 2015 ).…”

Section: D As a Neurotoxic Factormentioning

confidence: 99%

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Environmental exposure of the general population to cadmium as a risk factor of the damage to the nervous system: A critical review of current data

Ruczaj

Brzóska

2022

J of Applied Toxicology

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Nowadays, more and more attention has been focused on the risk of the neurotoxic action of cadmium (Cd) under environmental exposure. Due to the growing incidence of nervous system diseases, including neurodegenerative changes, and suggested involvement of Cd in their aetiopathogenesis, this review aimed to discuss critically this element neurotoxicity. Attempts have been made to recognize at which concentrations in the blood and urine Cd may increase the risk of damage to the nervous system and compare it to the risk of injury of other organs and systems. The performed overview of the available literature shows that Cd may have an unfavourable impact on the human's nervous system at the concentration >0.8 μg Cd/L in the urine and >0.6 μg Cd/L in the blood. Because such concentrations are currently noted in the general population of industrialized countries, it can be concluded that environmental exposure to this xenobiotic may create a risk of damage to the nervous system and be involved in the aetiopathogenesis of neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease, as well as worsening cognitive and behavioural functions. The potential mechanism of Cd neurotoxicity consists in inducing oxidative stress, disrupting the activity of enzymes essential to the proper functioning of the nervous system and destroying the homoeostasis of bioelements in the brain. Thus, further studies are necessary to recognize accurately both the risk of nervous system damage in the general population due to environmental exposure to Cd and the mechanism of this action.

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supporting

confidence: 68%

Section: D As a Neurotoxic Factormentioning

confidence: 99%

Environmental exposure of the general population to cadmium as a risk factor of the damage to the nervous system: A critical review of current data

Ruczaj

Brzóska

2022

J of Applied Toxicology

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“…Changes in the cristae ultrastructure during stress conditions leads to breakdown of interactive and communicative means between ETC proteins as well as diminished mitochondrial function and plasticity. Numerous reports using transmission electron microscopy (TEM) evidence deleterious effects of cadmium on mitochondrial cristae, such as reduction in number and shortening, in various animal systems (Asar et al 2004;Braeckman et al 1999;Early et al 1992;Ord et al 1988;Yang et al 2016) and has been correlated with reduced expression of cytochrome c oxidases (COX), essential components of ETC complexes, indicating compromised mitochondrial function (Takaki et al 2004;Toury et al 1985). In view of recent discoveries, future studies are required to elucidate the molecular targeting of cadmium on protein complexes that govern cristae organization.…”

Section: Mitochondrial Membranes: Ultrastructure and Lipid Compositionmentioning

confidence: 99%

Cell organelles as targets of mammalian cadmium toxicity

Lee

Thévenod

2020

Arch Toxicol

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Ever increasing environmental presence of cadmium as a consequence of industrial activities is considered a health hazard and is closely linked to deteriorating global health status. General animal and human cadmium exposure ranges from ingestion of foodstuffs sourced from heavily polluted hotspots and cigarette smoke to widespread contamination of air and water, including cadmium-containing microplastics found in household water. Cadmium is promiscuous in its effects and exerts numerous cellular perturbations based on direct interactions with macromolecules and its capacity to mimic or displace essential physiological ions, such as iron and zinc. Cell organelles use lipid membranes to form complex tightly-regulated, compartmentalized networks with specialized functions, which are fundamental to life. Interorganellar communication is crucial for orchestrating correct cell behavior, such as adaptive stress responses, and can be mediated by the release of signaling molecules, exchange of organelle contents, mechanical force generated through organelle shape changes or direct membrane contact sites. In this review, cadmium effects on organellar structure and function will be critically discussed with particular consideration to disruption of organelle physiology in vertebrates.

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Neurotoxicity of Metal Mixtures

Andrade

Aschner

Santos

2017

Advances in Neurobiology

128

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Metals are the oldest toxins known to humans. Metals differ from other toxic substances in that they are neither created nor destroyed by humans (Casarett and Doull's, Toxicology: the basic science of poisons, 8th edn. McGraw-Hill, London, 2013). Metals are of great importance in our daily life and their frequent use makes their omnipresence and a constant source of human exposure. Metals such as arsenic [As], lead [Pb], mercury [Hg], aluminum [Al] and cadmium [Cd] do not have any specific role in an organism and can be toxic even at low levels. The Substance Priority List of Agency for Toxic Substances and Disease Registry (ATSDR) ranked substances based on a combination of their frequency, toxicity, and potential for human exposure. In this list, As, Pb, Hg, and Cd occupy the first, second, third, and seventh positions, respectively (ATSDR, Priority list of hazardous substances. U.S. Department of Health and Human Services, Public Health Service, Atlanta, 2016). Besides existing individually, these metals are also (or mainly) found as mixtures in various parts of the ecosystem (Cobbina SJ, Chen Y, Zhou Z, Wub X, Feng W, Wang W, Mao G, Xu H, Zhang Z, Wua X, Yang L, Chemosphere 132:79-86, 2015). Interactions among components of a mixture may change toxicokinetics and toxicodynamics (Spurgeon DJ, Jones OAH, Dorne J-L, Svendsen C, Swain S, Stürzenbaum SR, Sci Total Environ 408:3725-3734, 2010) and may result in greater (synergistic) toxicity (Lister LJ, Svendsen C, Wright J, Hooper HL, Spurgeon DJ, Environ Int 37:663-670, 2011). This is particularly worrisome when the components of the mixture individually attack the same organs. On the other hand, metals such as manganese [Mn], iron [Fe], copper [Cu], and zinc [Zn] are essential metals, and their presence in the body below or above homeostatic levels can also lead to disease states (Annangi B, Bonassi S, Marcos R, Hernández A, Mutat Res 770(Pt A):140-161, 2016). Pb, As, Cd, and Hg can induce Fe, Cu, and Zn dyshomeostasis, potentially triggering neurodegenerative disorders, such as Alzheimer's disease (AD) and Parkinson's disease (PD). Additionally, changes in heme synthesis have been associated with neurodegeneration, supported by evidence that a decline in heme levels might explain the age-associated loss of Fe homeostasis (Atamna H, Killile DK, Killile NB, Ames BN, Proc Natl Acad Sci U S A 99(23):14807-14812, 2002).The sources, disposition, transport to the brain, mechanisms of toxicity, and effects in the central nervous system (CNS) and in the hematopoietic system of each one of these metals will be described. More detailed information on Pb, Mn, Al, Hg, Cu, and Zn is available in other chapters. A major focus of the chapter will be on Pb toxicity and its interaction with other metals.

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Microstructure and Ultrastructure Alterations in the Pallium of Immature Mice Exposed to Cadmium

Cited by 6 publications

References 26 publications

Environmental exposure of the general population to cadmium as a risk factor of the damage to the nervous system: A critical review of current data

Environmental exposure of the general population to cadmium as a risk factor of the damage to the nervous system: A critical review of current data

Cell organelles as targets of mammalian cadmium toxicity

Neurotoxicity of Metal Mixtures

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