Chlorophenol stress affects aromatic amino acid biosynthesis—a genome‐wide study

Yadav, Vikas; Shitiz, Kirti; Pandey, Rishi; Yadav, Jyoti

doi:10.1002/yea.1825

Cited by 16 publications

(7 citation statements)

References 43 publications

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“…Previous studies have reported that 2,4-DCP affected aromatic amino acid biosynthesis (Yadav et al, 2011) and directly bound to proteins, to interfere with their conformation (Zhang et al, 2011), suggesting that 2,4-DCP may have a proteotoxicity that causes ER stress (Gardner et al, 2013). Our recent study using mouse embryonic fibroblasts has proven the hypothesis that 2,4-DCP induces ER stress (Zhang et al, 2014b).…”

Section: Discussionmentioning

confidence: 64%

Endoplasmic reticulum stress is involved in 2,4-dichlorophenol-induced hepatotoxicity

Zhang

Chen

et al. 2016

J. Toxicol. Sci.

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-2,4-Dichlorophenol (2,4-DCP) is an environmental pollutant exhibiting a wide spectrum of toxic effects. We investigated the toxic effects and potential mechanisms underlying 2,4-DCP-induced hepatotoxicity. In vitro, 2,4-DCP caused hepatotoxicity manifested by a decrease in cell viability and inhibition of colony formation. Bip and CHOP expression was up-regulated at the mRNA and protein levels. Moreover, 2,4-DCP induced eIF2α phosphorylation and Xbp1 mRNA splicing, indicating that endoplasmic reticulum (ER) stress was activated after exposure of HL7702 cells to 2,4-DCP for 12 hr. Furthermore, the mitochondrial membrane potential collapsed and apoptosis was triggered after exposure to 2,4-DCP for 24 hr. In vivo, 2,4-DCP caused histological changes in the liver, and dramatically elevated the serum alanine transaminase (ALT) and aspartate aminotransferase (AST) levels of mice. ER stress was also triggered in the liver of mice on days 1 and 3. The ER stress inhibitor TUDCA could partly relieve the liver damage, as indicated by the restoration of serum ALT and AST levels. Taken together, our results demonstrated that ER stress may serve as an early warning mechanism against 2,4-DCP-induced hepatotoxicity, and severe ER stress may lead to apoptosis.

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Section: Discussionmentioning

confidence: 64%

Endoplasmic reticulum stress is involved in 2,4-dichlorophenol-induced hepatotoxicity

Zhang

Chen

et al. 2016

J. Toxicol. Sci.

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“…as well as by-products formed during chlorination of drinking water for disinfection [1][2][3]. Most of the CPs are recalcitrant to natural biotic and chemical degradation, and some are known toxins, mutagens, and carcinogens [4,5]. Their toxicity, recalcitrance, bioaccumulation, strong odor emission, and persistence can directly impact the health of humans and wildlife and have a potential threat through the contamination of water bodies [6,7].…”

Section: Introductionmentioning

confidence: 99%

Kinetics study on the oxidation of chlorophenols by permanganate

Shao

Zou

Wang

et al. 2016

Desalination and Water Treatment

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A B S T R A C TThe kinetics of the oxidation of chlorophenols (CPs) by potassium permanganate was studied in the present study, along with the changes in oxidant dosage, pH, temperature, and real water matrices. The reactions between permanganate and three kinds of CPs, i.e. 4-chlorophenol (4-MCP), 2,4-dichlorophenol (2,4-DCP), and 2,4,6-trichlorophenol (2,4,6-TCP), are second order overall and first-order with respect to each reactant. The degradation rates of the CPs increase with increasing permanganate dosage or temperature. pH plays an important role during permanganate oxidation. With the increase in pH from 4.0 to 10.0, the reaction rates of 4-MCP and 2,4-DCP decrease first and then increase, and finally decrease rapidly when pH > pK a , while the rates of 2,4,6-TCP decrease continuously. The degradation rates of the CPs are obviously higher in real water than in pure water. The reaction rate follows the order of 2,4,6-TCP > 2,4-DCP > 4-MCP under acidic conditions, and follows the reverse order under alkaline conditions in both pure water and real water.

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“…ER stress induced by organic pollutants is usually characterized by the up‐regulations of CHOP and Bip (Faria et al, ; Haberzettl et al, ; Chang et al, ). Previous studies reported that 2,4‐DCP could bind with protein to interfere its conformation (Zhang et al, ) and affect aromatic amino acid biosynthesis (Yadav et al, ), which hinted that 2,4‐DCP might have a proteotoxicity to cause ER stress. To prove this assumption, the expressions of Bip and CHOP were measured in this study, and our results showed that 2,4‐DCP significantly increased the expressions of these two ER stress markers both at mRNA and protein levels.…”

Section: Discussionmentioning

confidence: 99%

2,4‐dichlorophenol induces ER stress‐mediated apoptosis via eIF2α dephosphorylation in vitro

Zhang

et al. 2014

Environmental Toxicology

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2,4-Dichlorophenol (2,4-DCP) has been widely used to produce herbicides and pharmaceutical intermediates, which exhibits various toxic effects including apoptosis. However, the mechanisms underlying 2,4-DCP-induced apoptosis, especially mediated by endoplasmic reticulum (ER) stress, are still unknown. In the present study, the mouse embryonic fibroblasts (MEFs) were used as an in vitro model system to figure out whether 2,4-DCP could induce ER stress, and further to elucidate the role of ER stress in 2,4-DCP-induced apoptosis. The results showed that 2,4-DCP dramatically caused the decrease of cell viability, the increase of apoptotic cells, the collapse of mitochondrial membrane potential (MMP) and the activation of caspase-3, suggesting that 2,4-DCP did induce apoptosis. Meanwhile, 2,4-DCP acted similarly as ER stress agonist tunicamycin (Tu) to activate all three branches (IRE1α, ATF6 and eIF2α) of ER stress. Furthermore, repression of ER stress or inhibition of eIF2α dephosphorylation significantly alleviated 2,4-DCP-induced apoptosis. Taking these results together, the present study firstly showed that 2,4-DCP induced ER stress-mediated apoptosis via eIF2α dephosphorylation in mammalian cells. These findings will provide new insights into the mechanisms underlying apoptosis after chlorophenols exposure.

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Chlorophenol stress affects aromatic amino acid biosynthesis—a genome‐wide study

Cited by 16 publications

References 43 publications

Endoplasmic reticulum stress is involved in 2,4-dichlorophenol-induced hepatotoxicity

Endoplasmic reticulum stress is involved in 2,4-dichlorophenol-induced hepatotoxicity

Kinetics study on the oxidation of chlorophenols by permanganate

2,4‐dichlorophenol induces ER stress‐mediated apoptosis via eIF2α dephosphorylation in vitro

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