Cadmium toxicity: A role in bone cell function and teeth development

Ma, Yonggang; Di, Ran; Shi, Xueni; Zhao, Hongyan; Liu, Zongping

doi:10.1016/j.scitotenv.2020.144646

Cited by 103 publications

(47 citation statements)

References 94 publications

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“…As regard defective calcification in the present results, reports of CdCl2 affecting calcified tissue can contribute to explaining the observation of interglobular dentin at PND20 section indicating developmental defect in the calcified globules (Kakei et al, 2009). The possible underlying mechanism for these changes may be either indirectly through affecting the calcium and phosphorus storage in bone (Uchida et al, 2010) or directly through osteoblast dysfunction and apoptosis (Ma et al, 2021).…”

Section: Discussionsupporting

confidence: 64%

Toxic Effect of Cadmium Chloride Exposure on Teeth Development in Sprague Dawley Rats During Pregnancy

Elhindawy

Helmy

Moawad

2021

Zagazig Journal of Forensic Medicine

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Background: Cadmium chloride (CdCl2) is a widely spread environmental toxin with reported developmental toxicity. Aim:The aim of the present work was to investigate the developmental toxicity of CdCl2 on rats' first molar histological structure, teeth mineralization through osteocalcin staining and evaluating caspase-3 expression as potential target, both intrauterine and after birth. Methods: Adult male and female Sprague Dawley rats were mated. Pregnant rats were divided into 2 groups, control group received water and experimental group received CdCl2 (5mg/kg) by oral gavage from 7 th to 17 th day of pregnancy. Two rats from control group and 8 rats from experimental group were sacrificed at gestational day 17 (GD17). Fifteen pups were obtained in control group and 10 pups in CdCl2 group. The day of parturition was deigned to be postnatal day (PND) zero (PND 0). From control group, 13 pups were sacrificed at PND10, and 13 pups at PND 20. From experimental groups, 12 pups were sacrificed at PND10, and 11 pups at PND 20. In all pups, heads were obtained for examining maxillary first molars. Results: Sections from the CdCl2 group showed delayed development, mineralization, and eruption of first molar than the control group in GD17, PND10 and PND 20. As regard osteocalcin, the expression pattern was the same in both groups, but the intensity of the expression decreased within the CdCl2 group with statistically significant difference between them. In addition, caspase-3 expression increased indicating apoptosis induction. Conclusion: Exposure to CdCl2 during pregnancy can lead to delay in the developmental stages of the first molar teeth beside its effect on the mineralization of dentin, the delayed teeth eruption and inducing apoptosis is a possible pathway for these effects.

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Section: Discussionsupporting

confidence: 64%

Toxic Effect of Cadmium Chloride Exposure on Teeth Development in Sprague Dawley Rats During Pregnancy

Elhindawy

Helmy

Moawad

2021

Zagazig Journal of Forensic Medicine

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“…Previous epidemiological studies have clarified that increased Cd exposure correlates significantly with decreased bone mineral density and increased risk of fracture [ [20] , [21] , [22] , [23] , [24] , [25] , [26] , 61 ]. Furthermore, Cd might have direct toxic effects on bones [ 23 , 62 ]. Cd has been shown to inhibit the differentiation of bone marrow mesenchymal stem cells into osteoblasts, activate osteoclases, promote bone resorption, and induce osteoblast injury and apoptosis [ 62 ].…”

Section: Resultsmentioning

confidence: 99%

“…Furthermore, Cd might have direct toxic effects on bones [ 23 , 62 ]. Cd has been shown to inhibit the differentiation of bone marrow mesenchymal stem cells into osteoblasts, activate osteoclases, promote bone resorption, and induce osteoblast injury and apoptosis [ 62 ]. Other possible mechanisms have also been proposed, including Cd-induced renal tubular damage [ 61 ] with hypercalciuria [ 63 ] and demineralization of bones, and reduced generation of active vitamin D in renal tubular cells [ 64 , 65 ] with resultant decreased calcium uptake in the duodenum [ 66 ].…”

Section: Resultsmentioning

confidence: 99%

The preferential accumulation of cadmium ions among various tissues in mice

et al. 2022

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“…У лінії клітин, подібних до остеобластів миші, MC3T3-E1, дія 0,1-1 мкМ Cd знижувала активність клітинної лужної фосфатази, що є маркером диференціації остеобластів [26]. Більш того, підвищення концентрації понад 1 мкМ Cd збільшувало секрецію простагландину Е2 клітинами МС3Т3-Е1, що могло стимулювати утворення та активацію остеокластів та призводити до опосередкованої остеокластами кісткової резорбції [27,28]. Ці ефекти однозначно можуть викликати порушення нормального балансу між утворенням та резорбцією кісткової тканини.…”

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“…Дослідження показали, що поглинання Cd та цитотоксичність опосередковуються транзиторними потенційними рецепторними каналами 7 (TRPM7), пов'язаними з рецепторами, хоча проникність TRPM7 для Cd є слабкою. Автори також припустили, що дефіцит Ca 2+ або Mg 2+ , які переважно транспортуються TRPM7 [27], може посилити поглинання Cd в клітинах остеобластів.…”

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Multiple Effects of Chronic Low-Dose Cadmium Exposure on the Liver, Osteogenesis, and Hematopoiesis in Animals and Humans

Zemlianyi¹,

Gerasymchuk²,

Zaitsev³

et al. 2021

Ukr. ž. med. bìol. sportu

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Cadmium salts are among the TOP-20 of the most dangerous compounds for animals in terms of toxicity. At the same time, today there is a paradigm shift in the studies of cadmium effects: in contrast to the acute effects of intoxication, more importance and practical relevance is attained by studying the continued chronic exposure to small cadmium doses (Chronic Low Cd Exposure) which can take place in real environmental conditions of industrially polluted regions and already impacts about 10% of the world population. While the early changes in kidneys and marker parameters of the urinary system under the action of cadmium are being studied quite actively, cadmium effects on other organs and systems in the body are insufficiently investigated. The purpose of the study was to analyse the multiple effects of cadmium on liver function, osteogenesis, haematopoiesis, and haemostasis in animals and humans. Protective mechanisms that reduce cadmium accumulation in hepatocytes compared to renal cells, in particular, the role of cellular transporters of biogenic metal ions (Fe2+, Zn2+, Mn2+, Cu2+), are systematized. Results and discussion. Cadmium mostly uses divalent metal transporter 1 and Zrt/Irt-like transporters, such as ZIP8 and ZIP14. Given the role of liver in the chelation and deposition of cadmium in the form of complexes with metallothioneins and glutathione, the significant potential of chelating and antioxidant hepatoprotectants to reduce negative effects is suggested. The role of exogenous chemical chelators and antioxidants in detoxifying cadmium is supported by the studies of other cadmium-binding molecules (glutathione, polyphenols, anthocyanins). Both direct effects of cadmium on the osteogenesis and calcium metabolism, and indirect effects on osteoblasts and osteoclasts are considered. In particular, current data on cadmium role in the development of endemic disease Itai-Itai in Japan is discussed. Notably, cadmium effect in children has a special hazards and long-term consequences. Data on cadmium role in interfering Ca2+ metabolism, particularly its effects on epithelial calcium channels (TRPV5) and Na-phosphate co-transporters (SLC34A1) are summarized. Conclusion. Current data suggest that chronic effects of cadmium in ultra-low concentrations upon the osteogenesis are even more evident than in renal system. A review of current data on cadmium effects upon the hematopoietic system in animal models is presented. The earliest studies found relation between cadmium and haemoglobin decrease, which could be mediated by interfering with intracellular Fe traffic, and effects on erythropoietin synthesis. Cadmium affected haemostasis and increased platelet aggregation. Animal studies suggest that chronic cadmium toxicity leads to hypercoagulation and increases the risks of thrombosis. Based on the summarized data, it is concluded that the investigating cadmium effects on hematopoiesis and hemostasis is a promising area for further studies of chronic low-dose cadmium exposure

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Cadmium toxicity: A role in bone cell function and teeth development

Cited by 103 publications

References 94 publications

Toxic Effect of Cadmium Chloride Exposure on Teeth Development in Sprague Dawley Rats During Pregnancy

Toxic Effect of Cadmium Chloride Exposure on Teeth Development in Sprague Dawley Rats During Pregnancy

The preferential accumulation of cadmium ions among various tissues in mice

Multiple Effects of Chronic Low-Dose Cadmium Exposure on the Liver, Osteogenesis, and Hematopoiesis in Animals and Humans

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