Ubiquitous hazardous metal lead induces TNF-α in human phagocytic THP-1 cells: Primary role of ERK 1/2

Khan, Mohammad Imran; Islam, Najmul; Sahasrabuddhe, Amogh A.; Mahdi, Abbas Ali; Siddiqui, Huma; Ashquin, Mohd; Ahmad, Iqbal

doi:10.1016/j.jhazmat.2011.02.027

Cited by 13 publications

(8 citation statements)

References 48 publications

(49 reference statements)

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“…The mean HPG serum levels increased significantly in the LE group and insignificantly in the ME and HE groups. The increase in the serum levels of both proteins may be caused by the pro-inflammatory properties of lead [45]. Chang et al [46] reported that 1 μM lead upregulates the transcription of genes encoding cyclooxygenase-2 (COX-2) and cytosolic phospholipase A 2 in vascular smooth muscle cells.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Occupational Lead Exposure on Blood Levels of Zinc, Iron, Copper, Selenium and Related Proteins

Kasperczyk

Prokopowicz

Dobrakowski

et al. 2012

Biol Trace Elem Res

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The study objective was to evaluate the effect of occupational lead exposure on blood concentrations of zinc, iron, copper, selenium and proteins related to them, such as transferrin, caeruloplasmin and haptoglobin. The examined group consisted of 192 healthy male employees of zinc–lead works. By the degree of lead exposure, the exposed group was subdivided into three subgroups. The control group was composed of 73 healthy male administrative workers. The markers of lead exposure (blood levels of lead and zinc protoporphyrin) were significantly elevated in the exposed group compared with the control group. Additionally, concentrations of copper and caeruloplasmin were raised. The significant increase in haptoglobin level was observed only in the low exposure group. Selenium levels were significantly decreased, whereas iron, zinc and transferrin levels were unchanged in the exposed group compared with the control group. There were positive correlations between the lead toxicity parameters and the copper and caeruloplasmin levels. In conclusion, the effect of occupational exposure to lead on the metabolism of trace metals appears to be limited. However, significant associations between lead exposure and levels of copper and selenium were shown. Changed levels of positive acute-phase proteins, such as caeruloplasmin and haptoglobin, were also observed.

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Section: Discussionmentioning

confidence: 99%

The Effect of Occupational Lead Exposure on Blood Levels of Zinc, Iron, Copper, Selenium and Related Proteins

Kasperczyk

Prokopowicz

Dobrakowski

et al. 2012

Biol Trace Elem Res

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“…Mitogen‐activated protein kinases (MAPKs) are important intermediates in signal transduction pathways that are initiated by many types of cell surface receptors; they regulate cell functions including proliferation, gene expression, differentiation, mitosis, cell survival, and apoptosis . The ERK pathway is considered the classical, canonical MAPK signaling pathway . Caspases are a family of protease enzymes playing essential roles in programmed cell death (including apoptosis, pyroptosis, and necroptosis) and inflammation; they can mediate the apoptosis process by regulating the intracellular event cascade of proteases …”

Section: Resultsmentioning

confidence: 99%

Conformational and functional effects of MPA‐CdTe quantum dots on SOD: Evaluating the mechanism of oxidative stress induced by quantum dots in the mouse nephrocytes

Hao

Liu

2019

J of Molecular Recognition

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The application of quantum dots (QDs) is restricted by the biosafety issue. QDs contribute to the adverse effects of organisms probably because of the ability to induce oxidative stress via changing the activity of antioxidant enzyme, for example, superoxide dismutase (SOD). But the underlying molecular mechanisms still remain unclear. This study investigated the harmful effects of oxidative stress induced by mercaptopropionic acid capped CdTe QDs (MPA-CdTe QDs) on the mouse primary nephrocytes as well as the structure and function of SOD molecule and explored the underlying molecular mechanism. After 24-hour MPA-CdTe QD exposure, the activation level of extracellular regulated protein kinase (ERK) signaling pathway and cysteinyl-directed aspartate-specific proteases (Caspases) significantly increased, which led to the increasing level of reactive oxygen species (ROS) and cell apoptosis; the group pretreated with ROS scavenger N-acetyl-L-cysteine (NAC) significantly reduced the apoptotic cell percentage, indicating that ROS played a critical role in QD-induced cytotoxicity. Further molecular experiments showed that the interacting processes between the MPA-CdTe QDs and SOD were spontaneous which changed the conformation, secondary structure of SOD. The interaction significantly resulted in the tightening of polypeptide chains and the shrinkage of SOD, leading to the inhibition of molecular SOD activity. This study demonstrates the adverse effects of QDs, revealing their potential risk in biomedical applications.

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“…Chemokine (C-X-C motif) ligand 8 (CXCL8), tumor necrosis factor (TNF), and caspase-3 (CASP3) were hub proteins in the metal category. These proteins are reported as targets for metals (Carter et al, 1997;Khan et al, 2011;Kim et al, 2008), and they play important roles in tumor progression (Hamed et al, 2012;Knüpfer and Preiß, 2007). Because AR and poly (ADP-ribose) polymerase 1 (PARP1), which is associated with DNA repair and cellular differentiation (Tao et al, 2009;Vinggaard et al, 2000), were hub targets in the PAH category, we hypothesized that AR and PARP1 are important biomarkers for PAHs.…”

Section: Discussionmentioning

confidence: 99%

A network biology-based approach to evaluating the effect of environmental contaminants on human interactome and diseases

Iida

Takemoto

2018

Ecotoxicology and Environmental Safety

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Environmental contaminant exposure can pose significant risks to human health. Therefore, evaluating the impact of this exposure is of great importance; however, it is often difficult because both the molecular mechanism of disease and the mode of action of the contaminants are complex. We used network biology techniques to quantitatively assess the impact of environmental contaminants on the human interactome and diseases with a particular focus on seven major contaminant categories: persistent organic pollutants (POPs), dioxins, polycyclic aromatic hydrocarbons (PAHs), pesticides, perfluorochemicals (PFCs), metals, and pharmaceutical and personal care products (PPCPs). We integrated publicly available data on toxicogenomics, the diseasome, protein-protein interactions (PPIs), and gene essentiality and found that a few contaminants were targeted to many genes, and a few genes were targeted by many contaminants. The contaminant targets were hub proteins in the human PPI network, whereas the target proteins in most categories did not contain abundant essential proteins. Generally, contaminant targets and disease-associated proteins were closely associated with the PPI network, and the closeness of the associations depended on the disease type and chemical category. Network biology techniques were used to identify environmental contaminants with broad effects on the human interactome and contaminant-sensitive biomarkers. Moreover, this method enabled us to quantify the relationship between environmental contaminants and human diseases, which was supported by epidemiological and experimental evidence. These methods and findings have facilitated the elucidation of the complex relationship between environmental exposure and adverse health outcomes.

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Ubiquitous hazardous metal lead induces TNF-α in human phagocytic THP-1 cells: Primary role of ERK 1/2

Cited by 13 publications

References 48 publications

The Effect of Occupational Lead Exposure on Blood Levels of Zinc, Iron, Copper, Selenium and Related Proteins

The Effect of Occupational Lead Exposure on Blood Levels of Zinc, Iron, Copper, Selenium and Related Proteins

Conformational and functional effects of MPA‐CdTe quantum dots on SOD: Evaluating the mechanism of oxidative stress induced by quantum dots in the mouse nephrocytes

A network biology-based approach to evaluating the effect of environmental contaminants on human interactome and diseases

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