Phorate induced oxidative stress, DNA damage and differential expression of p53, apaf-1 and cat genes in fish, Channa punctatus (Bloch, 1793)

Ratn, Arun; Awasthi, Yashika; Kumar, Manoj; Singh, Sunil Kumar; Tripathi, Renu; Trivedi, Sunil P.

doi:10.1016/j.chemosphere.2017.05.008

Cited by 38 publications

(19 citation statements)

References 57 publications

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“…On the other hand, high levels of ROS are toxic to cells, due to their damage to cellular components [ 4 ]. In response to oxidative stress, there are alterations in the capacity of the antioxidant defense system in an attempt to minimize oxidative damage to cellular components, such as lipids, proteins and DNA [ 5 , 6 ]. Both eukaryotic and prokaryotic cells may protect themselves from ROS by producing antioxidant enzymes, including catalase, which degrades hydrogen peroxide, and superoxide dismutase (SOD), which dismutes superoxide [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

Trypsin Binding with Copper Ions Scavenges Superoxide: Molecular Dynamics-Based Mechanism Investigation

Zhong

Zhao

2018

IJERPH

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Trypsin is a serine protease, which has been proved to be a novel superoxide scavenger. The burst of superoxide induced by polychlorinated biphenyls can be impeded by trypsin in both wild type and sod knockout mutants of Escherichia coli. The experimental results demonstrated that the activities of superoxide scavenging of trypsin were significantly accelerated by Cu ions. Also, with the addition of Cu ions, a new β-sheet (β7) transited from a random coil in the Cu(II)-trypsin (TP) system, which was favorable for the formation of more contacts with other sheets of trypsin. Residue–residue network analysis and the porcupine plots proved that the Cu ion in trypsin strengthened some native interactions among residues, which ultimately resulted in much greater stability of the Cu(II)-TP system. Moreover, compact and stable trypsin structures with Cu ions might be responsible for significantly provoking the activity of superoxide scavenging.

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Section: Introductionmentioning

confidence: 99%

Trypsin Binding with Copper Ions Scavenges Superoxide: Molecular Dynamics-Based Mechanism Investigation

Zhong

Zhao

2018

IJERPH

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“…In vertebrates, Chen et al (2014) showed that there were no changes in the mRNA levels of this gene in liver cells of zebrafish (Danio rerio) exposed for 3 h to cadmium. In another study of D. rerio, Luzio et al (2013) observed that copper influenced the transcript levels of p53, and that individual organisms were capable of upregulating expression of this gene when the animals were exposed to this stressor for 6 h. Several other vertebrate studies have demonstrated similar results, indicating that upregulation of p53 mRNA levels is a common response of cells after exposure to different environmental contaminants (Xu et al 2008;Ratn et al 2017). For invertebrate species, Banni et al (2009) showed that mussels (Mytilus sp.)…”

Section: Discussionmentioning

confidence: 84%

Transcriptional levels of the cancer‐related genes p53, TAp63/73, and ∆Np63/73 in the blue mussel (Mytilus edulis) after lead exposure

Guerreiro

Rola

Almeida

et al. 2018

Invertebrate Biology

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The major role of the p53 gene family is related to the maintenance of genetic stability, protecting organisms from a wide range of stressors. Considering the importance of p53 in cancer development, this study aimed to analyze the expression of p53 isoforms in the mussel Mytilus edulis after lead exposure. We detected the p53 isoform both in the gills and in the digestive gland of mussels, but detected TAp63/73 and ∆Np63/73 isoforms only in the gills. Lead exposure induced upregulation of p53 mRNA levels in the digestive gland, without any effect in the gills. Conversely, mRNA levels of the TAp63/73 and ∆Np63/73 isoforms were downregulated in the gills after 1 d of exposure to lead. These results suggest that some similarities may exist between vertebrates and invertebrates and, specifically, that the balance between isoforms may represent a crucial step in cellular homeostasis. Moreover, the transcription of these cancer‐related genes seems to be regulated in a tissue‐ and time‐specific manner.

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“…The importance of inadequate expression of Apaf‐1 in tumorigenesis has been confirmed by multiple experimental observations . Early studies suggested that Apaf‐1 had some relationship with P53‐induced apoptosis . It is found that in human melanoma cells, these changes eventually led to the inactivation of Apaf‐1 due to allele deletion and/or promoter methylation‐dependent transcriptional silencing .…”

Section: Discussionmentioning

confidence: 93%

Apoptotic protease activating factor‐1 negatively regulates Wnt signaling in hepatocellular carcinoma

Han

Chen

2019

The Kaohsiung J of Med Scie

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The current study aims to evaluate the mechanism of apoptotic protease activating factor-1 (Apaf-1) in hepatocellular carcinoma (HCC) cells by verifying the regulation of the wnt/beta-catenin signaling pathway via Apal-1. Our data showed that transfection with Ad-Apaf-1 could inhibit the activity of a lymphoid enhancer factor (LEF) luciferase plasmid activated by β-catenin. Overexpressing Apaf-1 could suppress the β-catenin-induced LEF luciferase activity in a dose-dependent manner. Western blot assays demonstrated that the overexpression of Apaf1 significantly suppressed the expression of Wnt/β-catenin signaling-related proteins. Further study demonstrated that Apaf-1 suppressed HepG2 cell migration, invasion, and viability. Knocking down the expression of Apaf-1 activated the wnt/β-catenin pathway in HepG2 cells. In contrast, silencing β-catenin decreased the activation of wnt/β-catenin, even in the presence of si-Apaf-1. Cell cycle distribution analysis demonstrated a decrease in the number of cells in the G0/G1 phase in the Apaf-1 silencing group. In contrast, knocking down the expression of β-catenin increased the number of cells in the G0/G1 phase, even in the presence of si-Apaf-1. In summary, the Apaf-1-mediated suppression of HepG2 cell malignancy is achieved by inhibiting the wnt/β-catenin pathway.

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Phorate induced oxidative stress, DNA damage and differential expression of p53, apaf-1 and cat genes in fish, Channa punctatus (Bloch, 1793)

Cited by 38 publications

References 57 publications

Trypsin Binding with Copper Ions Scavenges Superoxide: Molecular Dynamics-Based Mechanism Investigation

Trypsin Binding with Copper Ions Scavenges Superoxide: Molecular Dynamics-Based Mechanism Investigation

Transcriptional levels of the cancer‐related genes p53, TAp63/73, and ∆Np63/73 in the blue mussel (Mytilus edulis) after lead exposure

Apoptotic protease activating factor‐1 negatively regulates Wnt signaling in hepatocellular carcinoma

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