Cadmium induces cytotoxicity in normal mouse renal MM55.K cells.
Jeong Doo HeoJu Hong LeeSeon Min LeeNa Hyun KimYeon Gyu MoonTae Kil TakMoonjung HyunJeong Doo HeoPublished in: International journal of environmental health research (2020)
The toxicity of cadmium (Cd) occurs through accumulation in the environment. The precise mechanism underlying Cd toxicity remains unclear. Therefore, in the present study, we studied the effects of Cd on MM55.K cells and investigated the mechanisms underlying Cd-induced cell death. CdCl2 significantly elevated apoptotic cell death, mitochondrial membrane potential (ΔΨm) loss, and caspase-dependent cell death. Moreover, immunoblotting results revealed that CdCl2 down-regulated the inhibitor of apoptotic protein such as survivin and Bcl-2 which led to the activation of caspase-3 and the cleavage of PARP in MM55.K cells. Besides, CdCl2 caused the up-regulation of ROS-related proteins such as HO-1 and ER stress-related proteins such as GRP78 and CHOP in MM55.K cells. CdCl2 toxicity resulted in the down-regulation of the AKT pathway that leads to the up-regulation of phosphorylated JNK and p38 in MM55.K cells. Thus, CdCl2 induce toxicity by AKT/MAPK regulation and causing ROS production, ER stress, ΔΨm loss, and apoptotic cell death in normal mouse renal cells.
Keyphrases
- cell death
- cell cycle arrest
- induced apoptosis
- oxidative stress
- signaling pathway
- endoplasmic reticulum stress
- pi k akt
- cell proliferation
- dna damage
- transcription factor
- risk assessment
- small molecule
- heavy metals
- diffuse large b cell lymphoma
- anti inflammatory
- reactive oxygen species
- high resolution
- human health
- endothelial cells
- binding protein
- oxide nanoparticles