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Cytoprotective effects of selenium on cadmium-induced LLC-PK1 cells apoptosis by activating JNK pathway

Yan Liu1, Shi-Ping Zhang, Yun-Qing Cai

  • 1Department of Nutrition and Food Hygiene, Nanjing Medical University, Nanjing 210029, People's Republic of China.

Toxicology in Vitro : an International Journal Published in Association with BIBRA
|March 27, 2007
PubMed

Insights

Selenium protects kidney cells from cadmium toxicity by reducing reactive oxygen species (ROS) and inhibiting the JNK pathway, which is involved in apoptosis. This study clarifies cadmium

Area of Science:

  • Cell Biology
  • Toxicology
  • Biochemistry

Background:

  • Cadmium exposure causes kidney damage (nephrotoxicity) linked to apoptosis and reactive oxygen species (ROS).
  • The exact cellular mechanisms of cadmium-induced apoptosis and potential protective agents are not fully understood.

Purpose of the Study:

  • To investigate the link between c-jun N-terminal kinase (JNK) activation and cadmium-induced apoptosis.
  • To evaluate selenium's potential to protect against cadmium-induced kidney cell damage.

Main Methods:

  • LLC-PK1 cells were treated with cadmium, with or without selenium pretreatment.
  • Analyzed JNK phosphorylation, caspase-3 activity, and ROS levels over time and with varying cadmium concentrations.

Main Results:

  • Cadmium induced apoptosis in LLC-PK1 cells, which was partially reduced by selenium.
  • Cadmium exposure increased JNK phosphorylation and caspase-3 activity in a dose- and time-dependent manner.
  • Selenium acted similarly to N-acetyl-L-cysteine (NAC), a free radical scavenger, by suppressing JNK phosphorylation and caspase-3 activation.

Conclusions:

  • Established a molecular connection between JNK phosphorylation and cadmium-induced apoptosis in kidney cells.
  • Demonstrated selenium's protective effect against cadmium cytotoxicity, likely through antioxidant mechanisms and JNK pathway modulation.

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