Cadmium-induced apoptosis in human normal liver L-02 cells by acting on mitochondria and regulating Ca2+ signals

Ye, Ji-Lin; Mao, Weiping; Wu, Ailian; Zhang, Nana; Zhang, Chao; Yu, Yang; Zhou, Lei; Wei, Caihong

doi:10.1016/j.etap.2007.01.007

Cited by 46 publications

(23 citation statements)

References 44 publications

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“…In the present study, we found that caspase-3 and caspase-9 activities were both increased in a concentration-dependent manner after Cd treatment, suggesting that caspase-3 and caspase-9 were required for apoptosis induced by Cd in testes of crabs. The activities of caspase-3 were observed significant increased in testes of crabs exposed to 116.00 mg·L −1 Cd compared to the control group, and these results were in agreement with Ye et al [61], indicating that apoptosis is characterized by a significant enhancement of caspase-3 activity. Caspase-9 located at the peak of caspase cascade activation, which is tarnally important for the activation of mitochondria-dependent apoptosis pathway [28].…”

Section: Discussionsupporting

confidence: 91%

Cadmium-Induced Oxidative Stress and Apoptotic Changes in the Testis of Freshwater Crab, Sinopotamon henanense

Wang

Lei

et al. 2011

PLoS ONE

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Cadmium (Cd), one of the most toxic environmental and industrial pollutants, is known to exert gonadotoxic and spermiotoxic effects. In the present study, we examined the toxic effect of Cd on the testis of freshwater crab, Sinopotamon henanense. Crabs were exposed to different Cd concentrations (from 0 to 116.00 mg·L−1) for 7 d. Oxidative stress and apoptotic changes in the testes were detected. The activities of SOD, GPx and CAT initially increased and subsequently decreased with increasing Cd concentrations, which was accompanied with the increase in malondialdehyde (MDA) and H2O2 content in a concentration-dependent manner. Typical morphological characteristic and physiological changes of apoptosis were observed using a variety of methods (HE staining, AO/EB double fluorescent staining, Transmission Electron Microscope observation and DNA fragmentation analysis), and the activities of caspase-3 and caspase-9 were increased in a concentration-dependent manner after Cd exposure. These results led to the conclusion that Cd could induced oxidative damage as well as apoptosis in the testis, and the apoptotic processes may be mediated via mitochondria-dependent apoptosis pathway by regulating the activities of caspase-3 and caspase-9.

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Section: Discussionsupporting

confidence: 91%

Cadmium-Induced Oxidative Stress and Apoptotic Changes in the Testis of Freshwater Crab, Sinopotamon henanense

Wang

Lei

et al. 2011

PLoS ONE

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“…]i) is a critical second messenger and regulator of cell apoptosis, a change in cytosolic-free Ca 2? leads to cell apoptosis through several own-stream mechanisms [11,12].…”

Section: Introductionmentioning

confidence: 99%

Surfactin Induces Apoptosis and G2/M Arrest in Human Breast Cancer MCF-7 Cells Through Cell Cycle Factor Regulation

Cao

Wang

Jiao

et al. 2009

Cell Biochem Biophys

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Surfactin, purified from Bacillus subtilis natto TK-1, inhibited proliferation of human breast cancer MCF-7 cells in a dose- and time-dependent manner, with IC(50) at 24, 48, and 72 h of 82.6, 27.3, and 14.8 microM, respectively. Surfactin-induced cell death was considered to be apoptotic by observing the typical apoptotic morphological change by acridine orange/ethidium bromide staining and Transferase-mediated dUTP Nick End-labeling assay. [Ca(2+)]i measurement revealed that surfactin induced a sustained increase in concentration of intracellular [Ca(2+)]i. Flow cytometric analysis also demonstrated that surfactin caused time-dependent apoptosis of MCF-7 cells through cell arrest at G(2)/M phase. Western blot revealed that surfactin induced accumulation of the tumor suppressor p53 and cyclin kinase inhibitor p21(waf1/cip1), and inhibited the activity of the G(2)-specific kinase, cyclin B1/p34(cdc2). Based on our findings, surfactin inhibited proliferation in MCF-7 cells by inducing apoptosis and the elevation of [Ca(2+)]i may play an important role in the apoptosis. The mechanism which surfactin caused G(2)/M arrest seems to be through cell cycle factor regulation.

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“…Some notable results have been reported regarding the potential cytotoxicity of QDs and related mechanism [18], [19], [20], [21]. Previous studies have shown that apoptosis is the major route of cell death in the case of cadmium cytotoxicity [22], [23]. It has also been suggested that induction of apoptosis is involved in cytotoxicity.…”

Section: Introductionmentioning

confidence: 99%

Determination of a Threshold Dose to Reduce or Eliminate CdTe-Induced Toxicity in L929 Cells by Controlling the Exposure Dose

et al. 2013

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With the widespread use of quantum dots (QDs), the likelihood of exposure to quantum dots has increased substantially. The application of quantum dots in numerous biomedical areas requires detailed studies on their toxicity. In this study, we aimed to determine the threshold dose which reduced or eliminated CdTe-induced toxicity in L929 cells by controlling the exposure dose. We established a cellular model of acute exposure to CdTe QDs. Cells were exposed to different concentrations of CdTe QDs (2.2 nm and 3.5 nm) followed by illustrative cytotoxicity analysis. The results showed that low concentrations of CdTe QDs (under 10 µg/mL) promoted cell viability, caused no obvious effect on the rate of cell apoptosis, intracellular calcium levels and changes in mitochondrial membrane potential, while high concentrations significantly inhibited cell viability. In addition, reactive oxygen species in the 10 µg/mL-treated group was significantly reduced compared with the control group. In summary, the cytotoxicity of CdTe QDs on L929 cell is dose-dependent, time-dependent and size-dependent. Low concentrations of CdTe QDs (below 10 µg/mL) may be nontoxic and safe in L929 cells, whereas high concentrations (above 10 µg/mL) may be toxic resulting in inhibition of proliferation and induction of apoptosis in L929 cells.

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Cadmium-induced apoptosis in human normal liver L-02 cells by acting on mitochondria and regulating Ca2+ signals

Cited by 46 publications

References 44 publications

Cadmium-Induced Oxidative Stress and Apoptotic Changes in the Testis of Freshwater Crab, Sinopotamon henanense

Cadmium-Induced Oxidative Stress and Apoptotic Changes in the Testis of Freshwater Crab, Sinopotamon henanense

Surfactin Induces Apoptosis and G2/M Arrest in Human Breast Cancer MCF-7 Cells Through Cell Cycle Factor Regulation

Determination of a Threshold Dose to Reduce or Eliminate CdTe-Induced Toxicity in L929 Cells by Controlling the Exposure Dose

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