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

Graniel-Amador, Mayra A.; Torres-Rodríguez, Héctor Fabián; Jiménez-Andrade, Juan Miguel; Hernández-Rodríguez, Joel; Arteaga-Silva, Marcela; Montes, Sergio

doi:10.1007/s10534-020-00265-x

Cited by 13 publications

(11 citation statements)

References 51 publications

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“…For example, Cd 2+ has been demonstrated to impair nervous tissue and different cell types including neurons and glial cells [ 16 , 17 , 18 ], thus representing one of the risk factors of neurodegenerative diseases including Parkinson’s disease and Alzheimer’s disease [ 14 , 19 , 20 ]. In addition, studies based on different animal models revealed significant associations between nerve damage and environmental exposure to Cd 2+ [ 21 , 22 , 23 , 24 ]. To gain more insights into the mechanisms of the pathogenesis of nerve damage caused by Cd, numerous molecular, biochemical, and structural studies have been carried out, and fundamental progress has been achieved.…”

Section: Introductionmentioning

confidence: 99%

Wnt/β-Catenin Signaling Pathway Is Strongly Implicated in Cadmium-Induced Developmental Neurotoxicity and Neuroinflammation: Clues from Zebrafish Neurobehavior and In Vivo Neuroimaging

Liu

Tian

et al. 2022

IJMS

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Cadmium (Cd) is a toxic heavy metal and worldwide environmental pollutant which seriously threatens human health and ecosystems. It is easy to be adsorbed and deposited in organisms, exerting adverse effects on various organs including the brain. In a very recent study, making full use of a zebrafish model in both high-throughput behavioral tracking and live neuroimaging, we explored the potential developmental neurotoxicity of Cd2+ at environmentally relevant levels and identified multiple connections between Cd2+ exposure and neurodevelopmental disorders as well as microglia-mediated neuroinflammation, whereas the underlying neurotoxic mechanisms remained unclear. The canonical Wnt/β-catenin signaling pathway plays crucial roles in many biological processes including neurodevelopment, cell survival, and cell cycle regulation, as well as microglial activation, thereby potentially presenting one of the key targets of Cd2+ neurotoxicity. Therefore, in this follow-up study, we investigated the implication of the Wnt/β-catenin signaling pathway in Cd2+-induced developmental disorders and neuroinflammation and revealed that environmental Cd2+ exposure significantly affected the expression of key factors in the zebrafish Wnt/β-catenin signaling pathway. In addition, pharmacological intervention of this pathway via TWS119, which can increase the protein level of β-catenin and act as a classical activator of the Wnt signaling pathway, could significantly repress the Cd2+-induced cell cycle arrest and apoptosis, thereby attenuating the inhibitory effects of Cd2+ on the early development, behavior, and activity, as well as neurodevelopment of zebrafish larvae to a certain degree. Furthermore, activation and proliferation of microglia, as well as the altered expression profiles of genes associated with neuroimmune homeostasis triggered by Cd2+ exposure could also be significantly alleviated by the activation of the Wnt/β-catenin signaling pathway. Thus, this study provided novel insights into the cellular and molecular mechanisms of Cd2+ toxicity on the vertebrate central nervous system (CNS), which might be helpful in developing pharmacotherapies to mitigate the neurological disorders resulting from exposure to Cd2+ and many other environmental heavy metals.

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Section: Introductionmentioning

confidence: 99%

Wnt/β-Catenin Signaling Pathway Is Strongly Implicated in Cadmium-Induced Developmental Neurotoxicity and Neuroinflammation: Clues from Zebrafish Neurobehavior and In Vivo Neuroimaging

Liu

Tian

et al. 2022

IJMS

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“…40,41 Previous studies have shown that cadmium exposure attenuates bone density and disrupts the microarchitecture of trabecular bone, which is regulated by bone cells, including osteoblasts and osteoclasts. 25,42 In addition, cadmium affects the activity of antioxidant enzymes (e.g., SOD, GSH-Px, and CAT) in bone tissue. 43 In the present study, we found that cadmium exposure impaired the total antioxidant activity in femur and tibia bones of rats.…”

Section: Discussionmentioning

confidence: 99%

Puerarin alleviates cadmium‐induced oxidative damage to bone by reducing autophagy in rats

Tong

Guo

Liu

et al. 2021

Environmental Toxicology

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Autophagy is a regulatory mechanism involved in cadmium (Cd)-induced bone toxicity and is suppressed by various stimuli, including oxidative stress. Puerarin is an isoflavonoid compound isolated from Pueraria, a plant used in traditional Chinese medicine. The underlying mechanisms of action of puerarin remain unclear. The objective of this study was to explore the mitigating effects of puerarin on cadmiuminduced oxidative damage in the bones of rats. Cadmium exposure increased oxidative damage in rat bones; this was markedly decreased by puerarin treatment, as demonstrated by changes in the activity of antioxidative enzymes. Cadmium-induced blockage of the expression of key bone regulatory proteins, autophagy-related markers, and signaling molecules was also alleviated by puerarin treatment. Additionally, cadmium reduced expression of the autophagic protein Rab7 and of late endosomal/lysosomal adaptor and MAPK and mTOR activator 1 (LAMTOR1); the decrease in these proteins was not restored by puerarin treatment. We speculate that puerarin relieves the inhibition of fusion of autophagosomes with lysosomes that is induced by cadmium; however, this specific effect of puerarin and downstream effects on bone regulatory mechanisms require further investigation. In conclusion, puerarin alleviates cadmium-induced oxidative damage in the bones of rats by attenuating autophagy, which is likely associated with the antioxidant activity of puerarin.

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“…As a result of Cd’s serious neurotoxicity, it can cause a series of neuropathy throughout the body. A study found that the lesions are mainly caused by embryonic transmission and respiratory pathways ( 92 – 95 ). Similarly, in addition to contributing to toxic effects on the peripheral nervous system, the absorbed Cd also damages olfactory neurons, central nervous cells, and oligodendrocytes through competitive replacement, as well as generates a large number of free radicals after entering the brain, which can induce many diseases including headache, dizziness, olfactory dysfunction, Parkinson-like symptoms, vasomotor control impairment, and learning impairment.…”

Section: The Possible Harm Of CD Exposure To the Bodymentioning

confidence: 99%

The function of omega-3 polyunsaturated fatty acids in response to cadmium exposure

Chen

Wang

et al. 2022

Front. Immunol.

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Throughout history, pollution has become a part of our daily life with the improvement of life quality and the advancement of industry and heavy industry. In recent years, the adverse effects of heavy metals, such as cadmium (Cd), on human health have been widely discussed, particularly on the immune system. Here, this review summarizes the available evidence on how Cd exposure may affect health. By analyzing the general manifestations of inflammation caused by Cd exposure, we find that the role of omega-3 (n-3) polyunsaturated fatty acids (PUFAs) in vivo can counteract Cd-induced harm. Additionally, we elucidate the effects of n-3 PUFAs on the immune system, and analyze their prophylactic and therapeutic effects on Cd exposure. Overall, this review highlights the role of n-3 PUFAs in the pathological changes induced by Cd exposure. Although n-3 PUFAs remain to be verified whether they can be used as therapeutic agents, as rehabilitation therapy, supplementation with n-3 PUFAs is reliable and effective.

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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

Cited by 13 publications

References 51 publications

Wnt/β-Catenin Signaling Pathway Is Strongly Implicated in Cadmium-Induced Developmental Neurotoxicity and Neuroinflammation: Clues from Zebrafish Neurobehavior and In Vivo Neuroimaging

Wnt/β-Catenin Signaling Pathway Is Strongly Implicated in Cadmium-Induced Developmental Neurotoxicity and Neuroinflammation: Clues from Zebrafish Neurobehavior and In Vivo Neuroimaging

Puerarin alleviates cadmium‐induced oxidative damage to bone by reducing autophagy in rats

The function of omega-3 polyunsaturated fatty acids in response to cadmium exposure

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