Triphenyl phosphate induced apoptosis of mice testicular Leydig cells and TM3 cells through ROS-mediated mitochondrial fusion inhibition

Wang, Minxin; Xu, Jinyu; Zhao, Zhengbo; Gong, Lirong; Su, Yu; Fang, Zhichao; Chen, Pengfei; Liu, Yifan; Zhang, Lianshuang; Xu, Feibo

doi:10.1016/j.ecoenv.2023.114876

Cited by 5 publications

(4 citation statements)

References 48 publications

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“…To further corroborate that acetylation of TauK274/281 induces apoptosis through mitochondrial fission, we administered another two drugs, Mitochondrial fusion promoter M1 (M1) (Wang et al., 2023) and metformin (Met) (Izzo et al., 2017), known to promote mitochondrial fusion, to HEK293 cells transfected with TauKQ. We observed that the individual administration of both drugs had no significant impact on mitochondrial dynamics‐related proteins.…”

Section: Resultsmentioning

confidence: 99%

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Acetylated tau exacerbates apoptosis by disturbing mitochondrial dynamics in HEK293 cells

Zhang,

Fang,

Zhao

et al. 2024

Journal of Neurochemistry

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An increase in tau acetylation at K274 and K281 and abnormal mitochondrial dynamics have been observed in the brains of Alzheimer's disease (AD) patients. Here, we constructed three types of tau plasmids, TauKQ (acetylated tau mutant, by mutating its K274/K281 into glutamine to mimic disease‐associated lysine acetylation), TauKR (non‐acetylated tau mutant, by mutating its K274/K281 into arginine), and TauWT (wild‐type human full‐length tau). By transfecting these tau plasmids in HEK293 cells, we found that TauWT and TauKR induced mitochondrial fusion by increasing the level of mitochondrial fusion proteins. Conversely, TauKQ induced mitochondrial fission by reducing mitochondrial fusion proteins, exacerbating mitochondrial dysfunction and apoptosis. BGP‐15 ameliorated TauKQ‐induced mitochondrial dysfunction and apoptosis by improving mitochondrial dynamics. Our findings suggest that acetylation of K274/281 represents an important post‐translational modification site regulating mitochondrial dynamics, and that BGP‐15 holds potential as a therapeutic agent for mitochondria‐associated diseases such as AD.

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Section: Resultsmentioning

confidence: 99%

“…no. HY‐100828, MCE), 1 μM Mitochondrial fusion promoter M1 (Wang et al., 2023) (Cat.no. HY‐111475) or 0.5 mM metformin (Izzo et al., 2017) (Cat.…”

Section: Methodsmentioning

confidence: 99%

Acetylated tau exacerbates apoptosis by disturbing mitochondrial dynamics in HEK293 cells

Zhang,

Fang,

Zhao

et al. 2024

Journal of Neurochemistry

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“…In 2018, OPFRs accounted for 30% of the global flame-retardant market as an alternative to brominated flame retardants ( 8 ). There are now multiple pathways for humans to become exposed to OPFRs due to the increased use of these particles in household dusts and food workers ( 19 ). OPFR is primarily transmitted through inhalation or dust inhalation in young children who spend most of their time at home, while food inhalation is predominant in adolescents and adults ( 20 ).…”

Section: Discussionmentioning

confidence: 99%

Integrative analysis of triphenyl phosphate: contextual interpretation of bladder cancer cohort

Zhang,

Huang,

Huang

et al. 2023

Front. Oncol.

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In recent years, organophosphate ester flame retardants (OPFRs) have emerged as preferred alternatives to brominated flame retardants (BFRs) in materials such as building supplies, textiles, and furnishings. Simultaneously, a notable surge in bladder cancer incidences has been observed globally, particularly in developed nations, placing it as the 10th most prevalent cancer type. Among the extensive OPFRs, the linkage between triphenyl phosphate (TPP) and bladder cancer remains inadequately investigated. Hence, our study endeavors to elucidate this potential association. We sourced transcriptome profiles and TPP-related data from The Cancer Genome Atlas and Comparative Toxicogenomics databases. Using the ssGSEA algorithm, we established TPP-correlated scores within the bladder cancer cohort. Differentially expressed analysis enabled us to identify key genes in bladder cancer patients. We utilized the LASSO regression analysis, along with univariate and multivariate COX regression analyses to construct a prognostic prediction model. To uncover critical pathways involving key genes, we employed GSEA and GSVA enrichment analyses. Molecular docking analysis was performed to determine the binding capability between TPP and proteins. Our findings reveal that the TPP-centric risk model offers valuable prediction for bladder cancer cohorts. Furthermore, the reliability of this TPP-influenced risk model was verified through ROC curve analysis and survival studies. Intriguingly, TPP exposure appears to bolster the proliferation and invasiveness of bladder cancer cells. This study furnishes new insights into the possible benefits of minimizing TPP exposure for hindering bladder cancer progression.

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“…Testosterone is the primary androgen in the male body, and its levels directly affect spermatogenesis [ 16 ]. Testosterone is primarily synthesized and secreted by Leydig cells in the testes through a series of enzymatic reactions.…”

Section: Testis Physiologymentioning

confidence: 99%

Hormone Regulation in Testicular Development and Function

Li,

Lin,

Wang

et al. 2024

IJMS

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The testes serve as the primary source of androgens and the site of spermatogenesis, with their development and function governed by hormonal actions via endocrine and paracrine pathways. Male fertility hinges on the availability of testosterone, a cornerstone of spermatogenesis, while follicle-stimulating hormone (FSH) signaling is indispensable for the proliferation, differentiation, and proper functioning of Sertoli and germ cells. This review covers the research on how androgens, FSH, and other hormones support processes crucial for male fertility in the testis and reproductive tract. These hormones are regulated by the hypothalamic–pituitary–gonad (HPG) axis, which is either quiescent or activated at different stages of the life course, and the regulation of the axis is crucial for the development and normal function of the male reproductive system. Hormonal imbalances, whether due to genetic predispositions or environmental influences, leading to hypogonadism or hypergonadism, can precipitate reproductive disorders. Investigating the regulatory network and molecular mechanisms involved in testicular development and spermatogenesis is instrumental in developing new therapeutic methods, drugs, and male hormonal contraceptives.

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Triphenyl phosphate induced apoptosis of mice testicular Leydig cells and TM3 cells through ROS-mediated mitochondrial fusion inhibition

Cited by 5 publications

References 48 publications

Acetylated tau exacerbates apoptosis by disturbing mitochondrial dynamics in HEK293 cells

Acetylated tau exacerbates apoptosis by disturbing mitochondrial dynamics in HEK293 cells

Integrative analysis of triphenyl phosphate: contextual interpretation of bladder cancer cohort

Hormone Regulation in Testicular Development and Function

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