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The protection of selenium on ROS mediated-apoptosis by mitochondria dysfunction in cadmium-induced LLC-PK(1) cells
Yi-Jing Zhou1, Shi-Ping Zhang, Chang-Wei Liu
1Department of Nutrition and Food Hygiene, Nanjing Medical University, 140 Han-zhong Road, Nanjing 210029, The People's Republic of China.
Abstract:
Selenium, an essential trace element, showed the significant protective effects against liver and kidney damage induced by some heavy metals. However, the mechanism how selenium suppresses cadmium (Cd)-induced cytotoxicity remains unclear. In this study, we investigated the protective mechanism of selenium on Cd-induced apoptosis in LLC-PK(1) cells via reactive oxygen species (ROS) and mitochondria linked signal pathway. Studies of PI and Annexin V dual staining analysis demonstrated that 20 microM Cd-induced apoptosis as early as 18 h. A concomitant by the generation of ROS, the loss of mitochondrial membrane potential, cytochrome c (cyt c) release, activation of caspase-9, -3 and regulation of Bcl-2 and Bax were observed. N-acetylcysteine (NAC, 500 microM), a free radical scavenger, was used to determine the involvement of ROS in Cd-induced apoptosis. During the process, selenium played the same role as NAC. The anti-apoptosis exerted by selenium involved the blocking of Cd-induced ROS generation, the inhibition of Cd-induced mitochondrial membrane potential collapse, the prevention of cyt c release, subsequent inhibition of caspase activation and the changed level of Bcl-2 and Bax. Taken together, we concluded that Cd-induced apoptosis was mediated by oxidative stress and selenium produced a significant protection against Cd-induced apoptosis in LLC-PK(1) via ameliorating the mitochondrial dysfunction.
Insights
Selenium protects against cadmium-induced cell damage by reducing oxidative stress and preserving mitochondrial function. This essential trace element prevents apoptosis by blocking reactive oxygen species generation and stabilizing mitochondria.
Area of Science:
- Toxicology
- Cell Biology
- Biochemistry
Background:
- Selenium is an essential trace element with known protective effects against heavy metal toxicity.
- The precise mechanisms by which selenium mitigates cadmium-induced cytotoxicity, particularly apoptosis, are not fully understood.
Purpose of the Study:
- To investigate the protective mechanism of selenium against cadmium-induced apoptosis in LLC-PK(1) cells.
- To elucidate the roles of reactive oxygen species (ROS) and mitochondrial signaling pathways in selenium's protective effects.
Main Methods:
- LLC-PK(1) cells were treated with cadmium (Cd) and/or selenium.
- Apoptosis was assessed using Propidium Iodide (PI) and Annexin V staining.
- Reactive oxygen species (ROS) generation, mitochondrial membrane potential, cytochrome c release, and caspase activation were measured.
- N-acetylcysteine (NAC) was used as a free radical scavenger control.
Main Results:
- Cadmium exposure induced apoptosis, characterized by increased ROS, loss of mitochondrial membrane potential, cytochrome c release, and caspase activation.
- Selenium treatment mirrored the effects of NAC, a ROS scavenger.
- Selenium inhibited Cd-induced ROS generation, mitochondrial dysfunction, cytochrome c release, and caspase activation, while modulating Bcl-2/Bax levels.
Conclusions:
- Cadmium-induced apoptosis in LLC-PK(1) cells is mediated by oxidative stress and mitochondrial dysfunction.
- Selenium confers significant protection against cadmium-induced apoptosis by ameliorating mitochondrial dysfunction and reducing oxidative stress.
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