Benzophenone 1 induced photogenotoxicity and apoptosis via release of cytochrome c and Smac/DIABLO at environmental UV radiation

Amar, Saroj Kumar; Goyal, Shruti; Dubey, Divya; Srivastav, Ajeet K.; Chopra, Deepti; Singh, Jyoti; Shankar, Jai; Chaturvedi, Rajnish Kumar; Ray, Ratan Singh

doi:10.1016/j.toxlet.2015.09.024

Cited by 43 publications

(25 citation statements)

References 42 publications

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“…We found that co-treatment with miR-382 and γδ T cells induced significant translocation of tBid to mitochondria through the c-FLIP/caspase 8 pathway ( Figure 5C). Since the translocation of tBid induced opening of mitochondrial permeability transition pore (mPTP) [21], we found that combination with miR-382 and γδ T cells induced release of cytochrome c and Smac/DIABLO, which were the apoptotic inducer [22], from mitochondria into the cytoplasm. As the results, caspase 9 and its substrate caspase 3 were significantly activated ( Figure 5D).…”

Section: Mir-382 Promotes γδ T Cells-induced Activation Of Caspases Tmentioning

confidence: 99%

WITHDRAWN: Overexpression of miR-382 sensitizes hepatocellular carcinoma cells to γδ T cells through inhibiting the expression of c-FLIP

Hou¹,

Chen²,

Zheng³

et al. 2018

Oncotarget

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Section: Mir-382 Promotes γδ T Cells-induced Activation Of Caspases Tmentioning

confidence: 99%

WITHDRAWN: Overexpression of miR-382 sensitizes hepatocellular carcinoma cells to γδ T cells through inhibiting the expression of c-FLIP

Hou¹,

Chen²,

Zheng³

et al. 2018

Oncotarget

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“…It was also upregulated 144 h after PH and may have been related to defective and/or excessive apoptosis of new cells and changes in liver volume. DIABLO promotes apoptosis (Amar et al, 2015) and was upregulated at multiple time points, indicating its functionality throughout the entire rat LR process. Ferredoxin reductase (FDXR) is a component of the cytochrome P-450 mitochondrial electron transport chain, and was downregulated during the entire LR process, indicating changes in mitochondrial biochemical activity and function.…”

Section: Discussionmentioning

confidence: 95%

Expression profiles of genes associated with mitochondria-mediated apoptosis and their roles in liver regeneration

Xing¹,

Li²,

Guo³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. Mitochondria are closely associated with cell survival, and it is of interest to determine whether apoptosis pathways, which are mediated by mitochondria, are involved in liver regeneration (LR). To identify the mechanisms underlying mitochondria-mediated apoptosis during rat LR, we used the Rat Genome 230 2.0 Array to investigate changes in gene expression. Next, we searched the GO and NCBI databases for genes associated with apoptosis mediated by mitochondria, and QIAGEN and KEGG databases for any related signaling pathways. The expression profile function (Et) was then used to calculate the activity level of known signaling pathways associated with apoptosis. The results revealed the expression of 436 genes associated with apoptosis signaling pathways, among which 152 were confirmed to be primarily related to LR. Overall, 99, 136, 95, and 91 genes were first expressed during the initiation [0.5-4 h after partial hepatectomy (PH)], G0/G1 transition (4-6 h after PH), cell proliferation (6-66 h after PH), and redifferentiation and structural reconstruction (66-144 h after PH) phases, demonstrating that LR-related genes were primarily induced in the initiation phase, and were then expressed across multiple phases. Analysis using the gene synergy formula (Et) showed that caspase-dependent and DNA fragment-related/unrelated pathways induced apoptosis in the early and late periods of LR, and the caspase-independent and DNA fragment-related/unrelated pathways almost in the whole process. Therefore, these results show that several apoptosis pathways regulate LR in rat.

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“…Later, cells were stained with PI (50 μg/mL) and incubated in the dark for 30 minutes before the analysis. Flow cytometry used to determine the cellular DNA content (BD FACS‐Influx) using program Cell Quest and Mod Fit software …”

Section: Methodsmentioning

confidence: 99%

Biochemical regulation and structural analysis of copper‐transporting ATPase in a human hepatoma cell line for Wilson disease

Agnihotry

Dhusia

Srivastav

et al. 2019

J of Cellular Biochemistry

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Hepatic copper levels differ among patients with Wilson disease (WD) and normal individuals depending on the dietary intake, copper bioavailability, and genetic factors. Copper chloride (CuCl2) caused dose‐dependent reduction in cell viability of human teratocarcinoma (HepG2) cell line, measured using the 3‐(4,5‐dimethyl‐2‐thiazolyl)‐2,5‐diphenyl‐2H‐tetrazolium bromide (MTT) assay. Cells were exposed to different concentrations of CuCl2 in log doses and maximum cell viability reduction was recorded at 15 µg/mL. Toxic dose of CuCl2 is potent inducer of reactive oxygen species (ROS). Apoptosis as a pattern of cell death was confirmed through sub‐G1 fraction and morphological changes such as mitochondrial depolarization, endoplasmic reticulum and lysosomal destabilization, phosphatidylserine translocation, and DNA damage. Our transcriptional and translational results strongly support apoptotic cell death. Using the available data present in dbSNP and bioinformatics tools, three nonsynonymous single nucleotide polymorphisms (nsSNPs) were identified as deleterious, reducing the stability of protein ATP7B. Structural analysis of native and mutant ATP7B proteins was investigated using molecular dynamics simulation (MDS) approach. Mutation in ATP7B gene might disturb the structural conformation and catalytic function of the ATP7B protein may be inducing WD. Hence, excess dietary intake of copper chloride must be avoided for safety of health to prevent from WD.

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Benzophenone 1 induced photogenotoxicity and apoptosis via release of cytochrome c and Smac/DIABLO at environmental UV radiation

Cited by 43 publications

References 42 publications

WITHDRAWN: Overexpression of miR-382 sensitizes hepatocellular carcinoma cells to γδ T cells through inhibiting the expression of c-FLIP

WITHDRAWN: Overexpression of miR-382 sensitizes hepatocellular carcinoma cells to γδ T cells through inhibiting the expression of c-FLIP

Expression profiles of genes associated with mitochondria-mediated apoptosis and their roles in liver regeneration

Biochemical regulation and structural analysis of copper‐transporting ATPase in a human hepatoma cell line for Wilson disease

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