Compartmentalized regulation of NAD+ by Di (2-ethyl-hexyl) phthalate induces DNA damage in placental trophoblast

Zhao, Shuai; Hong, Yun Soo; Liang, Yue-yue; Li, Xiaolu; Shen, Jiang-chuan; Sun, Congcong; Chu, Lingluo; Hu, J. F.; Wang, Hua; Xu, De-Xiang; Zhang, Shichen; Xu, Dianna; Xu, Tao; Zhao, Lingli

doi:10.1016/j.redox.2022.102414

Cited by 4 publications

(3 citation statements)

References 98 publications

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“…The upregulation of TXNIP leads to the accumulation of intracellular ROS and induces widespread DNA damage since TXNIP encodes the thioredoxin-binding protein, which is a tumor suppressor that inhibits the antioxidant function of thioredoxin. The upregulation of PARP1, which depletes NAD + and inhibits mitochondrial ATP synthesis, is associated with damaged DNA . In addition, the observed downregulation of MT-CYB and MT-ND2 in the SDT group further suggests that ROS have damaged the mitochondrial respiratory chain, depleted intracellular energy, and induced cell death .…”

Section: Results and Discussionmentioning

confidence: 93%

“…The upregulation of PARP1, which depletes NAD + and inhibits mitochondrial ATP synthesis, is associated with damaged DNA. 39 In addition, the observed downregulation of MT-CYB and MT-ND2 in the SDT group further suggests that ROS have damaged the mitochondrial respiratory chain, depleted intracellular energy, and induced cell death. 40 Because of the ROS burst induced by MCTH with US irradiation, intracellular homeostasis is disrupted, and the oxidative stress system is activated (Figure 7b).…”

Section: Resultsmentioning

confidence: 95%

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Boosting Sono-immunotherapy of Prostate Carcinoma through Amplifying Domino-Effect of Mitochondrial Oxidative Stress Using Biodegradable Cascade-Targeting Nanocomposites

Wang,

Li,

Niu

et al. 2024

ACS Nano

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Sono-immunotherapy faces challenges from poor immunogenicity and low response rate due to complex biological barriers. Herein, we prepared MCTH nanocomposites (NCs) consisting of disulfide bonds (S–S) doped mesoporous organosilica (MONs), Cu-modified protoporphyrin (CuPpIX), mitochondria-targeting triphenylphosphine (TPP), and CD44-targeting hyaluronic acid (HA). MCTH NCs efficiently accumulate at the tumor site due to the overexpressed CD44 receptors on the membrane of the cancer cells. Under the function of HAase and glutathione (GSH), MCTH degrades and exposes TPP to deliver CuPpIX to the mitochondrial site and induce a reactive oxygen species (ROS) burst in situ under ultrasound irradiations, thereby causing severe mitochondria dysfunction. This cascade-targeting ability of MCTH NCs not only reinforces oxidative stress in cancer cells but also amplifies immunogenic cell death (ICD) to stimulate the body’s immune response and alleviate the tumor immunosuppressive microenvironment. These NCs significantly enhance the infiltration of immune cells into the tumor, particularly CD8+ T cells, for a powerful antitumor sono-immunotherapy. The proposed cascade-targeting strategy holds promise for strengthening sono-immunotherapy for prostate cancer treatment and overcoming the limitations of traditional immunotherapy.

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Section: Results and Discussionmentioning

confidence: 93%

Section: Resultsmentioning

confidence: 95%

Boosting Sono-immunotherapy of Prostate Carcinoma through Amplifying Domino-Effect of Mitochondrial Oxidative Stress Using Biodegradable Cascade-Targeting Nanocomposites

Wang,

Li,

Niu

et al. 2024

ACS Nano

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“…High doses of DEHP caused IUGR and induced fetal malformations ( 220 ). DEHP exposure also damaged DNA in the trophoblast ( 221 ) and altered the placental receptor expression ( 222 ).…”

Section: Maternal Phthalate Exposure Endocrine Effects On Fetal Growt...mentioning

confidence: 99%

Modulation of fetoplacental growth, development and reproductive function by endocrine disrupters

Basak,

Varma,

Duttaroy

2023

Front. Endocrinol.

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Maternal endocrine homeostasis is vital to a successful pregnancy, regulated by several hormones such as human chorionic gonadotropin, estrogen, leptin, glucocorticoid, insulin, prostaglandin, and others. Endocrine stress during pregnancy can modulate nutrient availability from mother to fetus, alter fetoplacental growth and reproductive functions. Endocrine disrupters such as bisphenols (BPs) and phthalates are exposed in our daily life's highest volume. Therefore, they are extensively scrutinized for their effects on metabolism, steroidogenesis, insulin signaling, and inflammation involving obesity, diabetes, and the reproductive system. BPs have their structural similarity to 17-β estradiol and their ability to bind as an agonist or antagonist to estrogen receptors to elicit an adverse response to the function of the endocrine and reproductive system. While adults can negate the adverse effects of these endocrine-disrupting chemicals (EDCs), fetuses do not equip themselves with enzymatic machinery to catabolize their conjugates. Therefore, EDC exposure makes the fetoplacental developmental window vulnerable to programming in utero. On the one hand prenatal BPs and phthalates exposure can impair the structure and function of the ovary and uterus, resulting in placental vascular defects, inappropriate placental expression of angiogenic growth factors due to altered hypothalamic response, expression of nutrient transporters, and epigenetic changes associated with maternal endocrine stress. On the other, their exposure during pregnancy can affect the offspring's metabolic, endocrine and reproductive functions by altering fetoplacental programming. This review highlights the latest development in maternal metabolic and endocrine modulations from exposure to estrogenic mimic chemicals on subcellular and transgenerational changes in placental development and its effects on fetal growth, size, and metabolic & reproductive functions.

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Perillaldehyde alleviates polyQ‐induced neurodegeneration through the induction of autophagy and mitochondrial UPR in Caenorhabditis elegans

Fang,

Liu,

Gao

et al. 2024

BioFactors

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Huntington's disease (HD) is a fatal neurodegenerative disease associated with autophagy disorder and mitochondrial dysfunction. Here, we identified therapeutic potential of perillaldehyde (PAE), a monoterpene compound obtained from Perilla frutescens (L.) Britt., in the Caenorhabditis elegans (C. elegans) model of HD, which included lifespan extension, healthspan improvement, decrease in polyglutamine (polyQ) aggregation, and preservation of mitochondrial network. Further analyses indicated that PAE was able to induce autophagy and mitochondrial unfolded protein reaction (UPRmt) activation and positively regulated expression of associated genes. In lgg‐1 RNAi C. elegans or C. elegans with UPRmt‐related genes knockdown, the effects of PAE treatment on polyQ aggregation or rescue polyQ‐induced toxicity were attenuated, suggesting that its neuroprotective activity depended on autophagy and UPRmt. Moreover, we found that pharmacological and genetic activation of UPRmt generally protected C. elegans from polyQ‐induced cytotoxicity. Finally, PAE promoted serotonin synthesis by upregulating expression of TPH‐1, and serotonin synthesis and neurosecretion were required for PAE‐mediated UPRmt activation and its neuroprotective activity. In conclusion, PAE is a potential therapy for polyQ‐related diseases including HD, which is dependent on autophagy and cell‐non‐autonomous UPRmt activation.

show abstract

Compartmentalized regulation of NAD+ by Di (2-ethyl-hexyl) phthalate induces DNA damage in placental trophoblast

Cited by 4 publications

References 98 publications

Boosting Sono-immunotherapy of Prostate Carcinoma through Amplifying Domino-Effect of Mitochondrial Oxidative Stress Using Biodegradable Cascade-Targeting Nanocomposites

Boosting Sono-immunotherapy of Prostate Carcinoma through Amplifying Domino-Effect of Mitochondrial Oxidative Stress Using Biodegradable Cascade-Targeting Nanocomposites

Modulation of fetoplacental growth, development and reproductive function by endocrine disrupters

Perillaldehyde alleviates polyQ‐induced neurodegeneration through the induction of autophagy and mitochondrial UPR in Caenorhabditis elegans

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