Figure - available from: Biological Trace Element Research
This content is subject to copyright. Terms and conditions apply.
Light micrographs of the pallium from each group mice. a Photomicrograph of the pallium of normal mice. The microstructure of pallium layer is intact. b Photomicrograph of the pallium of mice treated with low-dose cadmium. ←: pia mater slightly separated from pallium layer, ↑: capillary quantity increased, →: cells of the slight vacuolar degeneration, ↖: a few granule cells of karyopyknosis. c,d Photomicrograph of pallium of mice treated with medium-dose cadmium. c ←: pia mater distinctly separated from pallium, ↑: capillary quantity increased, ↘: slightly swelling cells, ↖: granule cells of karyopyknosis, ↙: increasing apoptotic cells. d ↗: local hemorrhage, →: vacuolar degeneration cells, ↑: capillary quantity increased, ↘: slightly swelling cells, ↙: increasing apoptotic cells. e, f, g Photomicrograph of the pallium of mice treated with high-dose cadmium. e ↓: seriously congestive capillary under pia mater, →: vacuolar degeneration cells, ↑: capillary quantity increased, ↖: granule cells of karyopyknosis. f ▲: some hypertrophy cells, ↑: capillary quantity increased, ↙: increasing apoptotic cells. g ←: pia mater separated from pallium, ↗: local hemorrhage, △: inflammatory cells infiltration. Magnification, ×400 (a–g). Scale bars (a–g), 200 nm. There was HE staining
Source publication
The aim of this study was to investigate microstructure and ultrastructure alterations in the pallium of immature mice exposed to cadmium. Forty immature mice were randomly divided into control, 1/100 LD50 (1.87 mg/kg, low), 1/50 LD50 (3.74 mg/kg, medium), and 1/25 LD50 (7.48 mg/kg, high) dose groups. After oral cadmium exposure for 40 days, the pa...
Citations
... )(Ibiwoye et al., 2019;PM et al., 2019;Pulido et al., 2019;Yang et al., 2015Yang et al., , 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; T A B L E 2 Changes in the structure of the brain of experimental animals due to acute and subacute exposure to Cd ...
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 etiopathogenesis, 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 etiopathogenesis 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 homeostasis 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.
... 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. ...
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.
Ever increasing environmental cadmium presence consequent of industrial activities is considered a health hazard and is closely linked to deteriorating global health status as general animal cadmium exposure expands from cigarette smoke and ingestion of foodstuffs sourced from heavily polluted hotspots to widespread contaminated air and water, including cadmium-containing microplastics found in household water. Cadmium exerts myriads of cellular perturbances based on its abilities to directly interact with macromolecules and to mimic or displace essential physiological ions. Cell organelles are membrane-bound structures that form complex tightly regulated compartmentalized networks with specialized functions which are fundamental to life. Interorganellar communication is mediated either by release of signaling molecules, mechanical force through change in organelle shape or direct membrane contacts and is crucial to orchestrate correct cell behavior and adaptive stress responses. In this chapter, cadmium effects on organellar structure and function will be reviewed with particular consideration to disruption of organelle physiology in vertebrates. Mitochondrial dysfunction (electron transport chain, mitochondrial membrane potential, permeability transition), mitochondrial dynamics, intralumenal homeostasis and stress response in the endoplasmic reticulum, altered nuclear architecture and chromatin organization, lysosomal expansion, instability and membrane permeabilization, autophagic flux, and disruption of vesicle trafficking will be discussed in the context of cadmium.
Cadmium (Cd) is a toxic heavy metal that impairs the development of hematopoietic stem cells (HSC) in mice, yet the mechanism of how Cd influences HSC remains elusive. Herein, we show that Cd activated non-canonical Wnt signaling pathway to impair HSC function in mice. After exposure to 10 ppm Cd chloride (CdCl2) via drinking water for 3 months, C57BL/6 mice displayed aberrant HSC function, in that HSC from Cd-treated mice were less efficient in rescue of lethally irradiated hosts and less competitive under mixed chimeric condition. Further analyses indicated that the small GTPase cdc42 was activated and its distribution pattern was depolarized in HSC by Cd exposure, and inhibition of cdc42 by casin, a selective chemical inhibitor, recovered the HSC capacity in rescue assay and their potential for lymphopoiesis under competitive mixed chimeric assay. Cd interaction with HSC was sufficient to promote non-canonical Wnt signaling pathway, but not canonical Wnt signaling pathway, to drive cdc42 activation and further increase the expression of C/EBPα and decrease the expression of Hhex. Moreover, Cd-induced activation of non-canonical Wnt signaling pathway in HSC did not persist long-termly in the presence of a normal niche without Cd, in that the elevated non-canonical Wnt signaling by Cd was diminished in HSC in the BM of normal recipients receiving purified HSC from Cd-treated mice after 6 months post transplantation. Taken together, our study suggests that Cd activates cdc42 of non-canonical Wnt signaling pathway to impair HSC function, a previously unknown mechanism for Cd toxicity on HSC.
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).
