Early signs of oral and inhalative cadmium uptake in rats

Prigge, Elena-Sophie

doi:10.1007/bf00364654

Cited by 56 publications

(11 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, there is a fair number of studies on what can be referred to as ) results in respiratory effects that are similar to those observed after acute exposure [3,4,36,[38][39][40]. Pathology features such as pulmonary oedema and cell hyperplasia in the bronchoalveolar region have been observed in rats following chronic cadmium exposure [41,42].…”

Section: Long-term Exposurementioning

confidence: 99%

Cadmium in tobacco smokers: a neglected link to lung disease?

et al. 2018

View full text Add to dashboard Cite

Cadmium in tobacco smoke may contribute to the development of pulmonary emphysema. However, there is poor understanding of the mechanisms behind the pathogenic role of cadmium in this and other smoking-related lung diseases. The traditional focus on the total body burden of cadmium, estimated through analysis of urine, may not fully reflect the local burden of cadmium, since it is inhaled by smokers. Thus, assessing the local accumulation of cadmium in the lungs appears more relevant, given that there is tissue-specific retention of cadmium.In this review, we outline the principal sources of cadmium exposure and the clinical effects of occupational exposure. In addition, we review evidence on local cadmium and its association with alterations in innate immunity in tobacco smokers. Moreover, we scrutinise the data on cadmium as a cause of lung disease in translational models.We conclude that cadmium may contribute to smoking-related lung diseases, possibly via an altered redox balance and by making macrophages dysfunctional. However, there is a need for new studies on local cadmium levels and their relation to pathology in long-term tobacco smokers, as well as for more indepth studies on cellular and molecular mechanisms, to elucidate the importance of cadmium in smokingrelated lung diseases.

show abstract

Section: Long-term Exposurementioning

confidence: 99%

Cadmium in tobacco smokers: a neglected link to lung disease?

et al. 2018

View full text Add to dashboard Cite

show abstract

“…The decrease in body iron is directly related to cad mium ingestion and not secondary to reduced diet con sumption 25 . The increased destruction of erythrocytes under cadmium intoxication may also be a contribut ing factor 9,26 .…”

Section: Discussionmentioning

confidence: 99%

Hemotoxic effects of cadmium in normal and protein malnourished rats

Husain

2015

Toxicol. Environ. Health Sci.

View full text Add to dashboard Cite

Cadmium is chemically related to zinc and found wherever zinc occurs in nature. Cadmium is emitted to air and water by mines, metal foundries, viz. brass and industries using Cadmium in alkaline accumul ators, alloys, paints and plastics. Cadmium exposure results in increase of concentration of a protein, call ed metallothionein, which plays an important role in detoxification of heavy metals. In persons not expos ed to high amounts of cadmium, the concentration of cadmium in blood, bound mainly to red blood cells, is very small, less than 1 μg/100 mL whole blood. Gontzea and Popescu 1 revealed that rats reared on low protein (casein 8.8%) diet were more susceptible to the adverse effects (blood and liver enzyme para meters) of injected Cd, than control given a diet with 17.8% casein. The present study was conducted on rats maintained on normal (21% protein) and protein malnourished (8% protein) diets. Exposure to cad mium in growing rats induced structural anomalies in the erythrocytes and leukocytes. Microcytic hypo chromic anemia with erythrocytopenia and leuko cytopenia were evident. Protein malnutrition appears to enhance the vulnerability of the animals to these changes.

show abstract

“…Cd +2 is a well-known nephrotoxin and a member of a well-known class of nephrotoxicants that cause acute tubular necrosis (Alpers and Chang, 2015). Many of the early studies of Cd +2 -induced nephrotoxity both in animal models (Cha 1987; Itokawa et al 1974; Kawamura et al 1978; Kotsonis and Klaassen 1978; Prigge 1978) and in case reports (Beton et al, 1966; Chugh et al, 1994), describe necrosis as the morphologically discernable form of cell death (ATSDR 2012). The literature has been replete with studies characterizing the apoptotic mode of cell death in Cd +2 -induced nephrotoxicity (Fujiwara et al, 2012, Prozialeck et al, 2012), but clearly, necrosis is the predominant mode of cell death during acute exposure and this is similar to that of many acutely toxic nephrotoxins (Sharfuddin et al, 2016) with apoptosis being a contributing component.…”

Section: Discussionmentioning

confidence: 99%

Human renal tubular cells contain CD24/CD133 progenitor cell populations: Implications for tubular regeneration after toxicant induced damage using cadmium as a model

Shrestha

Somji

Sens

et al. 2017

Toxicology and Applied Pharmacology

View full text Add to dashboard Cite

The proximal tubules of the kidney are target sites of injury by various toxicants. Cadmium (Cd+2), an environmental nephrotoxicant can cause adverse effects and overt renal damage. To decipher the mechanisms involved in nephrotoxicity, an in vitro model system is required. Mortal cultures of human proximal tubule (HPT) cells have served, as models but are difficult to acquire and do not lend themselves to stable transfection. The immortalized human proximal tubule cell line HK-2, has served as a model but it lacks vectorial active transport and shows signs of lost epithelial features. Recently a new proximal tubule cell line was developed, the RPTEC/TERT1, and the goal of this study was to determine if this cell line could serve as a model to study nephrotoxicity. Global gene expression analysis of this cell line in comparison to the HK-2 and HPT cells showed that the RPTEC/TERT1 cells had gene expression patterns similar to HPT cells when compared to the HK-2 cells. The HPT and the RPTEC/TERT1 cell line had an increased population of stem/progenitor cells co-expressing CD24 and CD133 when compared to the HK-2 cells. The level of expression of cadherins, claudins and occludin molecules was also similar between the RPTEC/TERT1 and the HPT cells. Acute exposure to Cd+2 resulted in necrosis of the RPTEC/TERT1 cells when compared to the HK-2 cells which died by apoptosis. Thus, the RPTEC/TERT1 cells are similar to HPT cells and can serve as a good model system to study mechanisms involved in toxicant induced renal damage.

show abstract

Early signs of oral and inhalative cadmium uptake in rats

Cited by 56 publications

References 27 publications

Cadmium in tobacco smokers: a neglected link to lung disease?

Cadmium in tobacco smokers: a neglected link to lung disease?

Hemotoxic effects of cadmium in normal and protein malnourished rats

Human renal tubular cells contain CD24/CD133 progenitor cell populations: Implications for tubular regeneration after toxicant induced damage using cadmium as a model

Contact Info

Product

Resources

About