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Published on: June 24, 2018
Cadmium induces apoptosis in the human osteoblast-like cell line Saos-2
K G Coonse1, A J Coonts, E V Morrison
1Department of Biology, Albertson College of Idaho, Caldwell, Idaho 83605, USA.
Abstract:
Human exposure to the heavy metal cadmium has been associated with the development of bone diseases, including osteoporosis and osteomalacia. The mechanisms by which cadmium exerts a direct effect on bone remain unclear. Bone cells go through apoptosis for proper bone remodeling; therefore, it was hypothesized that cadmium disrupts this normal balance by inducing apoptosis. Human osteoblast-like cells (Saos-2) were treated with 10-200 muM cadmium chloride (CdCl2) and evaluated by trypan blue staining and phase-contrast microscopy. Exposure to CdCl2 resulted in decreased cell viability and changes in cell morphology characteristic of apoptosis. The role of apoptosis in cadmium-induced toxicity was further evaluated using the fluorescent marker annexin V, which detects externalization of cell membrane phosphatidylserine. Nuclear changes associated with apoptosis were assessed by Hoechst staining and a DNA fragmentation assay. A significant increase in annexin V-positive cells was observed following CdCl2 treatment. Nuclear changes associated with apoptosis, including marginalization and condensing of chromatin and DNA fragmentation, were also observed following CdCl2 treatment. Cadmium-induced apoptosis in Saos-2 cells was also accompanied by an increase in caspase-3 activity. The addition of the caspase-3 inhibitor N-acetyl-Asp-Glu-Val-Asp-aldehyde (Ac-DEVD-CHO) or the known cadmium chelating agent potassium bis(2-hydroxyethy)dithiocarbamate, (K[bhedtc]), blocked caspase-3 activation induced by cadmium. Collectively, this study has identified a role for apoptosis in cadmium-induced toxicity in bone cells, and provides insight for future studies on mechanisms underlying the disruption of apoptotic signaling cascades in bone and the relationship to bone disease.
Insights
Cadmium exposure induces apoptosis, or programmed cell death, in human bone cells. This finding clarifies how heavy metal toxicity contributes to bone diseases like osteoporosis.
Area of Science:
- Toxicology
- Cell Biology
- Bone Biology
Background:
- Heavy metal cadmium exposure is linked to bone diseases such as osteoporosis.
- The precise mechanisms of cadmium's direct impact on bone tissue are not fully understood.
- Apoptosis, or programmed cell death, is crucial for bone remodeling, suggesting cadmium might interfere with this process.
Purpose of the Study:
- To investigate the hypothesis that cadmium induces apoptosis in human bone cells.
- To elucidate the role of apoptosis in cadmium-induced bone cell toxicity.
- To identify the signaling pathways involved in cadmium-induced apoptosis in osteoblasts.
Main Methods:
- Human osteoblast-like Saos-2 cells were treated with varying concentrations of cadmium chloride (CdCl2).
- Cell viability and morphology were assessed using trypan blue staining and microscopy.
- Apoptosis was confirmed through annexin V staining, Hoechst staining, DNA fragmentation assays, and caspase-3 activity measurement.
Main Results:
- Cadmium chloride exposure significantly reduced cell viability and induced apoptotic morphology in Saos-2 cells.
- Increased annexin V-positive cells and characteristic nuclear changes, including DNA fragmentation, were observed.
- Cadmium treatment elevated caspase-3 activity, which was inhibited by a caspase-3 inhibitor and a cadmium chelator.
Conclusions:
- This study demonstrates that cadmium induces apoptosis in human bone cells.
- Apoptosis plays a significant role in cadmium-induced bone cell toxicity.
- Findings provide insights into the mechanisms of cadmium-related bone diseases and potential therapeutic targets.
