Related Experiment Video
Updated: May 12, 2026
Protocol to Create Chronic Wounds in Diabetic Mice
Published on: September 25, 2019
The protective effects of selenium on cadmium-induced oxidative stress and apoptosis via mitochondria pathway in mice
Abstract:
Selenium, an essential trace element, showed the significant protective effects against kidney damage induced by some heavy metals. Our previous research have found that the protection effects of selenium on ROS mediated-apoptosis by mitochondria dysfunction in cadmium (Cd)-induced LLC-PK1 cells. The present study as a continuation of our earlier one to investigate the protective effects and mechanism of selenium on Cd-induced apoptosis of kidney in vivo. Cadmium exposure increased the production of reactive oxygen species (ROS) and altered the levels of oxidative stress related biomarkers in kidney tissue. A concomitant by the loss of mitochondrial membrane potential, cytochrome c release and regulation of VDAC, Bcl-2 and Bax were observed. Apoptotic nature of cell death is confirmed by activation of caspase-3, which is also supported by histological examination. During the process, selenium played a beneficial role against Cd-induced renal damage. Pretreatment with selenium partially blocked Cd-induced ROS generation, inhibited Cd induced mitochondrial membrane potential collapse, prevented cytochrome c release, inhibited caspase activation and changed the level of VDAC, Bcl-2 and Bax. Combining all, results suggest that selenium has an ability to inhibit mitochondrial apoptotic pathway in oxidative stress mediated kidney dysfunction caused by cadmium.
Insights
Selenium protects kidneys from cadmium damage by inhibiting oxidative stress and mitochondrial apoptosis. This essential trace element prevents cell death pathways, safeguarding kidney function against heavy metal toxicity.
Area of Science:
- Toxicology
- Cell Biology
- Trace Element Research
Background:
- Heavy metals like cadmium (Cd) induce kidney damage through oxidative stress and apoptosis.
- Selenium, an essential trace element, has shown protective effects against heavy metal-induced cellular damage.
- Previous in vitro studies indicated selenium's role in mitigating reactive oxygen species (ROS)-mediated apoptosis in cadmium-exposed kidney cells.
Purpose of the Study:
- To investigate the protective effects and underlying mechanisms of selenium against cadmium-induced kidney apoptosis in vivo.
- To elucidate selenium's role in modulating oxidative stress and mitochondrial dysfunction in cadmium-induced renal damage.
Main Methods:
- In vivo animal model exposed to cadmium.
- Assessment of oxidative stress biomarkers and reactive oxygen species (ROS) production in kidney tissue.
- Evaluation of mitochondrial membrane potential, cytochrome c release, and expression of VDAC, Bcl-2, and Bax proteins.
- Confirmation of apoptosis via caspase-3 activation and histological examination.
- Administration of selenium as a pretreatment to assess its protective effects.
Main Results:
- Cadmium exposure significantly increased ROS production and altered oxidative stress markers in kidney tissue.
- Cadmium induced loss of mitochondrial membrane potential, cytochrome c release, and altered VDAC, Bcl-2, and Bax levels, confirming mitochondrial dysfunction and apoptosis.
- Apoptosis was further confirmed by caspase-3 activation and histological changes.
- Selenium pretreatment partially inhibited cadmium-induced ROS generation and mitochondrial dysfunction.
- Selenium prevented cytochrome c release, caspase activation, and normalized the levels of VDAC, Bcl-2, and Bax.
Conclusions:
- Selenium exhibits significant protective effects against cadmium-induced kidney damage in vivo.
- Selenium mitigates cadmium toxicity by inhibiting the mitochondrial apoptotic pathway.
- The protective mechanism involves reducing oxidative stress, preserving mitochondrial function, and blocking key apoptotic signaling molecules.
