Role of autophagy in di-2-ethylhexyl phthalate (DEHP)-induced apoptosis in mouse Leydig cells

Sun, Ying‐Yin; Shen, Jinrong; Zeng, Lin; Yang, Dan; Shao, Shuxin; Wang, Jinglei; Wei, Jie; Xiong, Junping; Chen, Jiaxiang

doi:10.1016/j.envpol.2018.08.089

Cited by 100 publications

(50 citation statements)

References 53 publications

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“…In addition, our results showed that treatment of cells with DEHP induced over generation of intracellular ROS that leads to a disturbance of redox status balance in cells. In agreement with our studies, a significant increase in ROS generation was observed in vivo and in vitro studies following DEHP treatment . ROS overproduction observed in this work is an index of oxidative stress installation that could be the result of the antioxidant system incapacity to neutralize the ROS overproduction.…”

Section: Discussionsupporting

confidence: 92%

“…As expected, in the present study, the MTT assay indicated that Abbreviations: GAPDH, glyceraldehyde 3-phosphate dehydrogenase; HO-1, heme oxygenase-1; Nrf2, NF-E2 related factor 2. significant increase in ROS generation was observed in vivo and in vitro studies following DEHP treatment. [44][45][46] ROS overproduction observed in this work is an index of oxidative stress installation that could be the result of the antioxidant system incapacity to neutralize the ROS overproduction. In our study, compared with those of the control group, the activities of SOD and CAT increased significantly in DEHP treated cells.…”

Section: Discussionmentioning

confidence: 89%

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Di (2‐ethylhexyl) phthalate induces cytotoxicity in HEK‐293 cell line, implication of the Nrf‐2/HO‐1 antioxidant pathway

Amara

Timoumi

Graiet

et al. 2019

Environmental Toxicology

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The di (2‐ethylhexyl) phthalate (DEHP) is a plasticizer used in the polyvinyl chloride industry. Human exposure to this plasticizer is inevitable and contributes to several side effects. In this study, we examined whether DEHP induces apoptosis and oxidative stress in embryonic kidney cells (HEK‐293) and whether the nuclear factor E2‐related factor 2 (Nrf‐2)/heme oxygenase‐1 (HO‐1) antioxidant pathway is involved in the pathogenesis of this process. We demonstrated that DEHP is cytotoxic to HEK‐293 cells. It causes oxidative damage through the generation of free radicals, induces lipid peroxidation, and alters superoxide dismutase and catalase activities. Simultaneously, DEHP treatment decreases the expression and the protein level of Nrf‐2 and HO‐1. Inhibition of the Nrf‐2/HO‐1 pathway is related to the mitochondrial pathway of apoptosis. This apoptotic process is characterized by a loss of mitochondrial transmembrane potential (ΔΨm) and upregulation of the expression of caspase‐3 mRNA as well as its protein level.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 89%

Di (2‐ethylhexyl) phthalate induces cytotoxicity in HEK‐293 cell line, implication of the Nrf‐2/HO‐1 antioxidant pathway

Amara

Timoumi

Graiet

et al. 2019

Environmental Toxicology

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“…Autophagy has been observed in human cells in response to various stimuli, such as chemicals or toxin . As one of programmed cell death (PCD), autophagy is a subcellular degradation pathway that plays a critical role in maintaining eukaryotic homeostasis and cell health .…”

Section: Discussionmentioning

confidence: 99%

“…Oxidative stress occurs when the balance between the antioxidants and prooxidants is broken in the body . Oxidative stress is shown to be induced by many chemicals and plays an important role in reproductive toxicity . It has been reported that oxidative stress is involved in TOCP‐induced liver damage and autophagy of mouse Leydig TM3 cells …”

Section: Introductionmentioning

confidence: 99%

“…14 Oxidative stress is shown to be induced by many chemicals [15][16][17] and plays an important role in reproductive toxicity. 18 It has been reported that oxidative stress is involved in TOCP-induced liver damage 8 and autophagy of mouse Leydig TM3 cells. 10 Tea has been consumed in the world for thousands of years, and drinking tea is helpful to health and can even prevent some Si Yanga and Shuxin Shao contributed equally to this work.…”

Section: Introductionmentioning

confidence: 99%

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Tea polyphenols alleviate tri‐ortho‐cresyl phosphate‐induced autophagy of mouse ovarian granulosa cells

Yang

Shao

Huang

et al. 2019

Environmental Toxicology

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Tri‐ortho‐cresyl phosphate (TOCP), a widely used plasticizer in industry, can cause female reproductive damage. Tea polyphenols (TPs) have multiple health effects via inhibiting oxidative stress. However, the reproductive protection of TPs in TOCP‐induced female reproductive system damage is yet to be elucidated. In the study, TOCP inhibited cell viability and induced autophagy of mouse ovarian granulosa cells; while TPs could rescue the inhibition of viability and induction of autophagy. 3‐MA, an autophagy inhibitor, could also rescue the inhibition of cell viability. These results indicated that TPs played a protective role in TOCP‐induced autophagy. Furthermore, TPs could inhibit the induction of oxidative stress of the cells by TOCP, which implying that TPs might alleviate TOCP‐induced autophagy via inhibiting oxidative stress. Furthermore, TPs could rescue TOCP‐induced autophagy and oxidative stress in the mouse ovarian tissues. Taken together, these results indicated that TPs could protect TOCP‐induced ovarian damage via inhibiting oxidative stress.

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Exposure to phthalates: germline dysfunction and aneuploidy

Henderson

Colaiácovo

2021

Prenatal Diagnosis

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Epidemiological studies continue to reveal the enduring impact of exposures to environmental chemicals on human physiology, including our reproductive health. Phthalates, a well characterized class of endocrine disrupting chemicals and commonly utilized plasticizers, are among one of the many toxicants ubiquitously present in our environment. Phthalate exposure has been linked to increases in the rate of human aneuploidy, a phenomenon that is detected in 0.3% of livebirths resulting in genetic disorders including trisomy 21, approximately 4% of stillbirths, and over 35% of miscarriages. Here we review recent epidemiological and experimental studies that have examined the role that phthalates play in germline dysfunction, including increases in apoptosis, oxidative stress, DNA damage, and impaired genomic integrity, resulting in aneuploidy. We will further discuss subject variability, as it relates to diet and polymorphisms, and the sexual dimorphic effects of phthalate exposure, as it relates to sex‐specific targets. Lastly, we discuss some of the conserved effects of phthalate exposure across humans, mammalian models and nonmammalian model organisms, highlighting the importance of using model organisms to our advantage for chemical risk assessment and unveiling potential mechanisms that underlie phthalate‐induced reproductive health issues across species.

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Role of autophagy in di-2-ethylhexyl phthalate (DEHP)-induced apoptosis in mouse Leydig cells

Cited by 100 publications

References 53 publications

Di (2‐ethylhexyl) phthalate induces cytotoxicity in HEK‐293 cell line, implication of the Nrf‐2/HO‐1 antioxidant pathway

Di (2‐ethylhexyl) phthalate induces cytotoxicity in HEK‐293 cell line, implication of the Nrf‐2/HO‐1 antioxidant pathway

Tea polyphenols alleviate tri‐ortho‐cresyl phosphate‐induced autophagy of mouse ovarian granulosa cells

Exposure to phthalates: germline dysfunction and aneuploidy

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