Di-(2-ethylhexyl) phthalate inhibits DNA replication leading to hyperPARylation, SIRT1 attenuation, and mitochondrial dysfunction in the testis

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Di-(2-ethylhexyl) phthalate inhibits DNA replication leading to hyperPARylation, SIRT1 attenuation, and mitochondrial dysfunction in the testis. / Li, Xiaolin; Fang, Evandro Fei; Scheibye-Knudsen, Morten; Cui, Honghua; Qiu, Lu; Li, Jian; He, Yuping; Huang, Jing; Bohr, Vilhelm A.; Ng, Tzi Bun; Guo, Hongwei.

In: Scientific Reports, Vol. 4, 6434, 2014.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Li, X, Fang, EF, Scheibye-Knudsen, M, Cui, H, Qiu, L, Li, J, He, Y, Huang, J, Bohr, VA, Ng, TB & Guo, H 2014, 'Di-(2-ethylhexyl) phthalate inhibits DNA replication leading to hyperPARylation, SIRT1 attenuation, and mitochondrial dysfunction in the testis', Scientific Reports, vol. 4, 6434. https://doi.org/10.1038/srep06434

APA

Li, X., Fang, E. F., Scheibye-Knudsen, M., Cui, H., Qiu, L., Li, J., ... Guo, H. (2014). Di-(2-ethylhexyl) phthalate inhibits DNA replication leading to hyperPARylation, SIRT1 attenuation, and mitochondrial dysfunction in the testis. Scientific Reports, 4, [6434]. https://doi.org/10.1038/srep06434

Vancouver

Li X, Fang EF, Scheibye-Knudsen M, Cui H, Qiu L, Li J et al. Di-(2-ethylhexyl) phthalate inhibits DNA replication leading to hyperPARylation, SIRT1 attenuation, and mitochondrial dysfunction in the testis. Scientific Reports. 2014;4. 6434. https://doi.org/10.1038/srep06434

Author

Li, Xiaolin ; Fang, Evandro Fei ; Scheibye-Knudsen, Morten ; Cui, Honghua ; Qiu, Lu ; Li, Jian ; He, Yuping ; Huang, Jing ; Bohr, Vilhelm A. ; Ng, Tzi Bun ; Guo, Hongwei. / Di-(2-ethylhexyl) phthalate inhibits DNA replication leading to hyperPARylation, SIRT1 attenuation, and mitochondrial dysfunction in the testis. In: Scientific Reports. 2014 ; Vol. 4.

Bibtex

@article{c8be147b3b6048669e2afe110b446d2c,
title = "Di-(2-ethylhexyl) phthalate inhibits DNA replication leading to hyperPARylation, SIRT1 attenuation, and mitochondrial dysfunction in the testis",
abstract = "Di-(2-ethylhexyl)-phthalate (DEHP) is a ubiquitously used endocrine disruptor.There is widespread exposure to DEHP in the general population which has raised substantial public concern due to its potential detrimental health effects. It is particularly pertinent to investigate the molecular mechanisms of its testicular toxicity which are largely unknown. By feeding male rats DEHP for 2 weeks, rat spermatogenesis became disrupted, resulting in a decreased number of spermatocytes and spermatids. Since rapidly dividing tissues appeared to be particularly vulnerable to DEHP toxicity we investigated the effect of DEHP on DNA replication. Intriguingly, DEHP appeared to inhibit DNA replication as evidenced by results of fiber tract analysis. This led to induction of the mitochondrial apoptotic pathways and increased ROS production. Furthermore, the toxicity of DEHP led to respiratory chain defects and attenuation of ATP level probably brought about by hyperPARylation and undermined SIRT1 activity. Our findings reveal a previously unknown mitochondrial dysfunction in DEHP-induced testicular toxicity and highlight the importance of SIRT1 in male reproduction.",
author = "Xiaolin Li and Fang, {Evandro Fei} and Morten Scheibye-Knudsen and Honghua Cui and Lu Qiu and Jian Li and Yuping He and Jing Huang and Bohr, {Vilhelm A.} and Ng, {Tzi Bun} and Hongwei Guo",
year = "2014",
doi = "10.1038/srep06434",
language = "English",
volume = "4",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - Di-(2-ethylhexyl) phthalate inhibits DNA replication leading to hyperPARylation, SIRT1 attenuation, and mitochondrial dysfunction in the testis

AU - Li, Xiaolin

AU - Fang, Evandro Fei

AU - Scheibye-Knudsen, Morten

AU - Cui, Honghua

AU - Qiu, Lu

AU - Li, Jian

AU - He, Yuping

AU - Huang, Jing

AU - Bohr, Vilhelm A.

AU - Ng, Tzi Bun

AU - Guo, Hongwei

PY - 2014

Y1 - 2014

N2 - Di-(2-ethylhexyl)-phthalate (DEHP) is a ubiquitously used endocrine disruptor.There is widespread exposure to DEHP in the general population which has raised substantial public concern due to its potential detrimental health effects. It is particularly pertinent to investigate the molecular mechanisms of its testicular toxicity which are largely unknown. By feeding male rats DEHP for 2 weeks, rat spermatogenesis became disrupted, resulting in a decreased number of spermatocytes and spermatids. Since rapidly dividing tissues appeared to be particularly vulnerable to DEHP toxicity we investigated the effect of DEHP on DNA replication. Intriguingly, DEHP appeared to inhibit DNA replication as evidenced by results of fiber tract analysis. This led to induction of the mitochondrial apoptotic pathways and increased ROS production. Furthermore, the toxicity of DEHP led to respiratory chain defects and attenuation of ATP level probably brought about by hyperPARylation and undermined SIRT1 activity. Our findings reveal a previously unknown mitochondrial dysfunction in DEHP-induced testicular toxicity and highlight the importance of SIRT1 in male reproduction.

AB - Di-(2-ethylhexyl)-phthalate (DEHP) is a ubiquitously used endocrine disruptor.There is widespread exposure to DEHP in the general population which has raised substantial public concern due to its potential detrimental health effects. It is particularly pertinent to investigate the molecular mechanisms of its testicular toxicity which are largely unknown. By feeding male rats DEHP for 2 weeks, rat spermatogenesis became disrupted, resulting in a decreased number of spermatocytes and spermatids. Since rapidly dividing tissues appeared to be particularly vulnerable to DEHP toxicity we investigated the effect of DEHP on DNA replication. Intriguingly, DEHP appeared to inhibit DNA replication as evidenced by results of fiber tract analysis. This led to induction of the mitochondrial apoptotic pathways and increased ROS production. Furthermore, the toxicity of DEHP led to respiratory chain defects and attenuation of ATP level probably brought about by hyperPARylation and undermined SIRT1 activity. Our findings reveal a previously unknown mitochondrial dysfunction in DEHP-induced testicular toxicity and highlight the importance of SIRT1 in male reproduction.

UR - http://www.scopus.com/inward/record.url?scp=84923304409&partnerID=8YFLogxK

U2 - 10.1038/srep06434

DO - 10.1038/srep06434

M3 - Journal article

VL - 4

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

M1 - 6434

ER -

ID: 172128493