Cadmium‐induced toxicity is rescued by curcumin: A review

Mohajeri, Mohammad; Rezaee, Mehdi; Sahebkar, Amirhossein

doi:10.1002/biof.1376

Cited by 67 publications

(36 citation statements)

References 223 publications

(268 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…By contrast, the predominant responsive pathway for CdCl 2 , PFOA, TBBPA and tBHQ is the Nrf2/StRE signalling as there was no observable or insignificant induction of reporter activity in the pGL4.38‐ Cyp2a5_ StREMut cells. These observations align with the current understanding of the mechanism of action of these chemicals .…”

Section: Resultssupporting

confidence: 86%

Cyp2a5 Promoter‐based Gene Reporter Assay: A Novel Design of Cell‐based Bioassay for Toxicity Prediction

Abu-Bakar

Lang³

2018

Basic Clin Pharma Tox

View full text Add to dashboard Cite

The murine cytochrome P450 2a5 (Cyp2a5) gene is regulated by complex interactions of various stress-activated transcription factors (TFs). Elevated Cyp2a5 transcription under chemical-induced stress conditions is achieved by interplay between the various TFs - including as aryl hydrocarbon receptor (AhR) and nuclear factor (erythroid-derived 2)-like 2 wild-type (Nrf2) - at the 'stress-responding' cluster of response elements on the Cyp2a5 promoter, as well as through mRNA stabilization mediated by interaction of the stress-activated heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) with the 3'-UTR of the CYP2A5 mRNA. We designed a unique toxicity pathway-based reporter assay to include regulatory regions from both the 5' and the 3' untranslated regions of Cyp2a5 in a luciferase reporter plasmid to reflect in vivo responses to chemical insult. Human breast cancer MCF-7 cells were stably transfected with pGL4.38-Cyp2a5_Wt3k (wild-type) or mutant - pGL4.38-Cyp2a5_StREMut and pGL4.38-Cyp2a5_XREMut - reporter gene to monitor chemical-induced cellular response mediated by AhR and Nrf2 signalling. The recombinant cells were treated with representative of AhR agonist, polycyclic aromatic hydrocarbons, brominated flame retardant, fluorosurfactant, aromatic organic compound and metal, to determine the sensitivity of the Cyp2a5 promoter-based gene reporter assays to chemical insults by measuring the LC and EC of the respective chemicals. The three assays are sensitive to sublethal cellular responses of chemicals, which is an ideal feature for toxicity pathway-based bioassay for toxicity prediction. The wild-type reporter responded well to chemicals that activate crosstalk between the AhR and Nrf2, whilst the mutant reporters effectively gauge cellular response driven by either Nrf2/StRE or AhR/XRE signalling. Thus, the three gene reporter assays could be used tandemly to determine the predominant toxicity pathway of a given compound.

show abstract

Section: Resultssupporting

confidence: 86%

Cyp2a5 Promoter‐based Gene Reporter Assay: A Novel Design of Cell‐based Bioassay for Toxicity Prediction

Abu-Bakar

Lang³

2018

Basic Clin Pharma Tox

View full text Add to dashboard Cite

show abstract

“…The heavy metal cadmium (Cd 2+ ) is extensively found in food materials due to its industrial use. Environmental and occupational exposure to Cd 2+ may be an important risk factor for a broad spectrum of illnesses affecting body organs such as the liver, kidneys, and cardiovascular systems [27]. Growing evidence suggests that oxidative stress induced by Cd 2+ alters the free radical-scavenging effects of N -acetyl cysteine, resulting in cellular damage via increasing genome mutations and recombination, and accelerating lipid peroxidation [23].…”

Section: Resultsmentioning

confidence: 99%

Antioxidant Activity Evaluation of Dietary Flavonoid Hyperoside Using Saccharomyces Cerevisiae as a Model

et al. 2019

View full text Add to dashboard Cite

Oxidative stress leads to various diseases, including diabetes, cardiovascular diseases, neurodegenerative diseases, and even cancer. The dietary flavonol glycoside, hyperoside (quercetin-3-O-galactoside), exerts health benefits by preventing oxidative damage. To further understand its antioxidative defence mechanisms, we systemically investigated the regulation of hyperoside on oxidative damage induced by hydrogen peroxide, carbon tetrachloride, and cadmium in Saccharomyces cerevisiae. Hyperoside significantly increased cell viability, decreased lipid peroxidation, and lowered intracellular reactive oxygen species (ROS) levels in the wild-type strain (WT) and mutants gtt1∆ and gtt2∆. However, the strain with ctt1∆ showed variable cell viability and intracellular ROS-scavenging ability in response to the hyperoside treatment upon the stimulation of H2O2 and CCl4. In addition, hyperoside did not confer viability tolerance or intercellular ROS in CdSO4-induced stress to strains of sod1∆ and gsh1∆. The results suggest that the antioxidative reactions of hyperoside in S. cerevisiae depend on the intercellular ROS detoxification system.

show abstract

“…Upon Cd inhalation, the lungs are the main affected target and develop lung tumors, pulmonary fibrosis and emphysema. Some studies performed in animal models showed that, in response to acute exposition of rats to Cd salts, the evoked inflammatory process may induce a dose-related increase in lung LPO as measured by total lung TBARS levels [96].…”

Section: And Lipid Peroxidationmentioning

confidence: 99%

Cadmium-Induced Oxidative Stress: Focus on the Central Nervous System

et al. 2020

View full text Add to dashboard Cite

Cadmium (Cd), a category I human carcinogen, is a well-known widespread environmental pollutant. Chronic Cd exposure affects different organs and tissues, such as the central nervous system (CNS), and its deleterious effects can be linked to indirect reactive oxygen species (ROS) generation. Since Cd is predominantly present in +2 oxidation state, it can interplay with a plethora of channels and transporters in the cell membrane surface in order to enter the cells. Mitochondrial dysfunction, ROS production, glutathione depletion and lipid peroxidation are reviewed in order to better characterize the Cd-elicited molecular pathways. Furthermore, Cd effects on different CNS cell types have been highlighted to better elucidate its role in neurodegenerative disorders. Indeed, Cd can increase blood–brain barrier (BBB) permeability and promotes Cd entry that, in turn, stimulates pericytes in maintaining the BBB open. Once inside the CNS, Cd acts on glial cells (astrocytes, microglia, oligodendrocytes) triggering a pro-inflammatory cascade that accounts for the Cd deleterious effects and neurons inducing the destruction of synaptic branches.

show abstract

Cadmium‐induced toxicity is rescued by curcumin: A review

Cited by 67 publications

References 223 publications

Cyp2a5 Promoter‐based Gene Reporter Assay: A Novel Design of Cell‐based Bioassay for Toxicity Prediction

Cyp2a5 Promoter‐based Gene Reporter Assay: A Novel Design of Cell‐based Bioassay for Toxicity Prediction

Antioxidant Activity Evaluation of Dietary Flavonoid Hyperoside Using Saccharomyces Cerevisiae as a Model

Cadmium-Induced Oxidative Stress: Focus on the Central Nervous System

Contact Info

Product

Resources

About