Benzo[a]pyrene-induced necrosis in the HepG2 cells via PARP-1 activation and NAD+ depletion

Lin, Tao; Yang, M. S.

doi:10.1016/j.tox.2007.12.020

Cited by 36 publications

(25 citation statements)

References 42 publications

(52 reference statements)

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“…the externalization of phosphatidylserine (Balasubramanian et al, 2007). Compared to control cell populations, changes to nuclei lipids in the biofingerprint spectral region may be an IR biomarker of chemical-induced necrosis and apoptosis in cells (Lin and Yang, 2008).…”

Section: Discussionmentioning

confidence: 99%

Distinguishing nuclei-specific benzo[a]pyrene-induced effects from whole-cell alterations in MCF-7 cells using Fourier-transform infrared spectroscopy

2015

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Exposure to chemicals such as benzo[a]pyrene (B[a]P) can generate intracellular toxic mechanisms. Fourier-transform infrared (FTIR) spectroscopy is a novel approach that allows the non-destructive analysis of underlying chemical bond alterations in patho-physiological processes. This study set out to examine whether B[a]P-induced whole cell alterations could be distinguished from effects on nuclei of exposed cells. Using attenuated total reflection FTIR (ATR-FTIR) spectroscopy, alterations in nuclei isolated from B[a]P-treated MCF-7 cells concentrated either in G0/G1- or S-phase were observed. B[a]P-induced effects in whole-cells included alterations to lipids, DNA and protein spectral regions. Absorbance areas for protein and DNA/RNA regions in B[a]P-treated whole cells differed significantly (P<0.0001) from vehicle controls and these observations correlated with alterations noted in isolated nuclei. Our findings provide evidence that FTIR spectroscopy has the ability to identify specific chemical-induced alterations.

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Section: Discussionmentioning

confidence: 99%

Distinguishing nuclei-specific benzo[a]pyrene-induced effects from whole-cell alterations in MCF-7 cells using Fourier-transform infrared spectroscopy

2015

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“…PARP-1 is a nuclear enzyme activated by DNA damage, participating in DNA repair, the regulation of transcription, DNA replication, and cell death [41,42]. Over-activation of PARP-1 in response to excessive DNA damage rapidly depletes intracellular ATP [43]. Moreover, there is considerable in vitro evidence showing that H 2 O 2 rapidly and efficiently induces formation of single-strand breaks in the nuclear DNA of exposed cells [17,44].…”

Section: Discussionmentioning

confidence: 99%

Apoptosis-inducing factor plays a critical role in caspase-independent, pyknotic cell death in hydrogen peroxide-exposed cells

et al. 2009

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It has been proposed that continuously generated hydrogen peroxide (H(2)O(2)) inhibits typical apoptosis and instead initiates an alternate, apoptosis-inducing factor (AIF)-dependent process. Aside from the role of AIF, however, the detailed morphological characterization of H(2)O(2)-induced cell death is not complete. This study examined the cellular mechanism(s) by which the continuous presence of H(2)O(2) induces cell death. We also further analyzed the precise role of AIF by inhibiting its expression with siRNA. Exposure of cells to H(2)O(2) generated by glucose oxidase caused mitochondrion-mediated, caspase-independent cell death. In addition, H(2)O(2) exposure resulted in cell shrinkage and chromatin condensation without nuclear fragmentation, indicating that H(2)O(2) stimulates a pyknotic cell death. Further analysis of AIF-transfected cells clearly demonstrated that nuclear translocation of AIF is the most important event required for nuclear condensation, phosphatidyl serine translocation, and ultimately cell death in H(2)O(2)-exposed cells. Furthermore, ATP was rapidly and severely depleted in cells exposed to H(2)O(2) generated by glucose oxidase but not by H(2)O(2) added as a bolus. Suppression of the H(2)O(2)-mediated ATP depletion by 3-aminobenzamide led to a significant increase of nuclear fragmentation in glucose oxidase-exposed cells. Collectively, these findings suggest that an acute energy reduction by H(2)O(2) causes caspase-independent and AIF-dependent cell death.

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“…Recent studies have suggested the links between benzo[a]pyrene toxicity with cancer and cell death. Benzo[a]pyrene can cause cell death via either apoptosis [25] or necrosis [26], which are two different modes of cell death following exposure to the toxicant. The occurrence of the different modes of cell death depends on energy level.…”

Section: Investigation On Benzo[a]pyrene Toxicity Through the Determimentioning

confidence: 99%

“…Despite a decrease in total adenosine nucleotide (TAN) level, ATP/TAN was significantly increased together with a significant decrease in ADP/TAN prior to the loss of mitochondrial function [31]. Exposure to the same cell line to benzo[a]pyrene caused cell death via necrosis [26]. Therefore, determination of energy metabolites in the cells following benzo[a]pyrene exposure may lend support to the hypothesis that energy level is important in mediating the modes of cell death.…”

Section: Investigation On Benzo[a]pyrene Toxicity Through the Determimentioning

confidence: 99%

Analysis of adenosine phosphates in HepG-2 cell by a HPLC–ESI-MS system with porous graphitic carbon as stationary phase

Wang

Lin

Lai

et al. 2009

Journal of Chromatography B

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Benzo[a]pyrene-induced necrosis in the HepG2 cells via PARP-1 activation and NAD+ depletion

Cited by 36 publications

References 42 publications

Distinguishing nuclei-specific benzo[a]pyrene-induced effects from whole-cell alterations in MCF-7 cells using Fourier-transform infrared spectroscopy

Distinguishing nuclei-specific benzo[a]pyrene-induced effects from whole-cell alterations in MCF-7 cells using Fourier-transform infrared spectroscopy

Apoptosis-inducing factor plays a critical role in caspase-independent, pyknotic cell death in hydrogen peroxide-exposed cells

Analysis of adenosine phosphates in HepG-2 cell by a HPLC–ESI-MS system with porous graphitic carbon as stationary phase

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