Cadmium induces apoptosis in human embryonic kidney (HEK) 293 cells by caspase-dependent and -independent pathways acting on mitochondria

Mao, Weiping; Ye, Ji-Lin; Zhang, Guan; Zhao, Jie-Ming; Zhang, Chao; Zhang, Nana; Jiang, Ping; Tian, Ting

doi:10.1016/j.tiv.2006.09.004

Cited by 99 publications

(61 citation statements)

References 42 publications

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“…Other cells in brain, such as neuronal cells of the cortex and hypothalamus and neuron-glia cultures are also sensitive to Cd (Yang et al, 2007b), but astrocytes are crucial to survival and repair of all these cell types. HEK 293 cells in comparison are more resilient than either HepG2 or 1321N1 cells at low concentrations of Cd, but as shown previously, CdCl 2 decreases viability in a time and dose dependent manner, and causes significant cell damage at high concentrations (Mao et al, 2007). Overall, these results indicate a differential sensitivity, likely due to differences in the underlying protective mechanisms present in each cell type.…”

Section: Discussionsupporting

confidence: 59%

Differential sensitivity and responsiveness of three human cell lines HepG2, 1321N1 and HEK 293 to cadmium

Lawal

Ellis

2010

J. Toxicol. Sci.

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-Cadmium (Cd) is a toxic heavy metal with no uniform mechanism of toxicity. In this the present study, the toxic effect of 5, 10 and 50 μM of Cd chloride was compared in three human cell lines; a human hepatoma cell line HepG2, a human astrocytoma cell line 1321N1, and a human embryonic kidney cell HEK 293. The results indicate a decrease in the viability of all three cell lines following exposure to Cd with HepG2 cells (IC 50 = 13.96 μM) showing the most sensitivity when measured using the MTT assay. There was significant increase in lactate dehydrogenase leakage, DNA damage, malondialdeyde and antioxidant enzymes activities in all three cell lines especially at 50 μM Cd. Significant decreases in ATP production were also observed at all Cd concentrations in HepG2 and HEK 293 cell lines. ROS levels significantly increase and GSH/GSSG ratio significantly decrease in all the three cell lines after Cd exposure, but these effects were attenuated by the presence of N-acetylcysteine (NAC). The present study therefore shows that ROS production and glutathione (GSH) depletion may play a role in Cd-induced toxicity in all the three cell lines. The endogenous levels of protective enzymes as well as their responsiveness are likely to determine a cell's susceptibility to Cd.

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Section: Discussionsupporting

confidence: 59%

Differential sensitivity and responsiveness of three human cell lines HepG2, 1321N1 and HEK 293 to cadmium

Lawal

Ellis

2010

J. Toxicol. Sci.

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“…Two distinct pathways of apoptosis have been identified: mitochondria-initiated apoptosis that occurs through caspase-9 and the death receptor-mediated pathway that requires caspase-8 (32). Caspase-3 is a key effecter molecule in the caspase-dependent cell apoptosis pathway that cleaves a number of cellular proteins, leading to apoptotic changes.…”

Section: Discussionmentioning

confidence: 99%

HJC, a New Arylnaphthalene Lignan Isolated From Justicia procumbens, Causes Apoptosis and Caspase Activation in K562 Leukemia Cells

2014

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Abstract. The aim of this study is to investigate whether HJC, isolated from Justicia procumbens for the first time, can suppress the proliferation and induce apoptosis of human leukemia K562 cells and finally clarify its related mechanism. The chemical structure of HJC was validated by LC-ESI-MS/MS, cytotoxicity was assayed using MTT, and apoptosis was investigated by flow cytometry. These assays indicated that HJC remarkably inhibited the growth in K562 cells by decreasing cell proliferation, reducing the SOD activity, enhancing ROS levels and inducing apoptosis. Activation of caspase-3 indicated that HJC may be inducing intrinsic and extrinsic apoptosis pathways and that HJC-induced apoptosis was caspase-dependent. This study suggests that HJC is a high-potency anti-tumor agent, and it induces apoptosis through a caspase-dependent pathway in human leukemia K562 cells. It also presents a potential alternative to leukemia therapy.

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“…Studies have shown that cadmium may trigger cell death by caspase-dependent and/or independent apoptotic mechanisms, depending on cell types (Coutant et al, 2006;Mao et al, 2007). Resveratrol was able to potentially improve the cell viability and markedly down-regulate cadmium induced robust up-regulation of caspase-3.…”

Section: Discussionmentioning

confidence: 99%

Resveratrol inhibits cadmium induced neuronal apoptosis by modulating calcium signalling pathway via regulation of MAPK/mTOR network

Lin¹,

Peng²,

Yang³

et al. 2015

Bangladesh J Pharmacol

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Cadmium, a toxic environmental contaminant, induces oxidative stress leading to various neurodegenerative disorders, where it interferes with homeos-tasis of intracellular free calcium ([Ca2+]i), leading to cellular damage and apoptosis. We investigated whether resveratrol, a plant-derived antioxidant could offer protection against cadmium-induced neuroapoptosis. Primary cortical neurons were exposed to cadmium (10 or 20 µM) with/without prior exposure to resveratrol (5, 10 or 20 µM) for 12 hours and unexposed cells served as control. Resveratrol caused marked reduction in cadmium-induced neuronal apoptosis and down-regulated caspase-3 expressions. Cadmium-induced marked elevations in reactive oxygen species, and ([Ca2+]i) levels were potentially reduced by resveratrol. Resveratrol effectively regulated the alterations observed in the activation levels of mitogen-activated protein kinases (MAPKs) and proteins of mammalian target of rapamycin (mTOR) pathways. Thus, resveratrol effectively protected the cortical neurons exposed to cadmium by modulating the ([Ca2+]i) levels and regulating the MAPK/mTOR pathways.

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Cadmium induces apoptosis in human embryonic kidney (HEK) 293 cells by caspase-dependent and -independent pathways acting on mitochondria

Cited by 99 publications

References 42 publications

Differential sensitivity and responsiveness of three human cell lines HepG2, 1321N1 and HEK 293 to cadmium

Differential sensitivity and responsiveness of three human cell lines HepG2, 1321N1 and HEK 293 to cadmium

HJC, a New Arylnaphthalene Lignan Isolated From Justicia procumbens, Causes Apoptosis and Caspase Activation in K562 Leukemia Cells

Resveratrol inhibits cadmium induced neuronal apoptosis by modulating calcium signalling pathway via regulation of MAPK/mTOR network

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