The plasticizer BBP selectively inhibits epigenetic regulator sirtuins

Zhang, Jian; Ali, Hamed I.; Bedi, Yudhishtar S.; Choudhury, Mahua

doi:10.1016/j.tox.2015.10.004

Cited by 20 publications

(17 citation statements)

References 66 publications

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“…For instance, livers from rats exposed to sodium arsenite (25 ppm) presented reduced levels of Nrf1, Nrf2 and Tfam, and Ppargc1a (PGC-1α) and diminished expression and activity of mitochondrial complexes (Prakash & Kumar 2016). In human liver HepG2 cells and C3H10T1/2 mesenchymal stem cells, the plasticizer benzyl butyl phthalate (BBP, 1 nM-50 μM) also downregulated the expression of NRF1, NRF2, TFAM and PPARGC1A (Zhang et al 2015b, Zhang & Choudhury 2017. Additionally, levels of sirtuins (SIRT) 1 and 3, two NAD +dependent deacetylases with different roles in the control of mitochondrial biogenesis (Nogueiras et al 2012), were also decreased.…”

Section: Mdcs and Mitochondrial Biogenesismentioning

confidence: 99%

Mitochondria as target of endocrine-disrupting chemicals: implications for type 2 diabetes

Marroquí

Tudurí

Alonso-Magdalena

et al. 2018

Journal of Endocrinology

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Type 2 diabetes is a chronic, heterogeneous syndrome characterized by insulin resistance and pancreatic β-cell dysfunction or death. Among several environmental factors contributing to type 2 diabetes development, endocrine-disrupting chemicals (EDCs) have been receiving special attention. These chemicals include a wide variety of pollutants, from components of plastic to pesticides, with the ability to modulate endocrine system function. EDCs can affect multiple cellular processes, including some related to energy production and utilization, leading to alterations in energy homeostasis. Mitochondria are primarily implicated in cellular energy conversion, although they also participate in other processes, such as hormone secretion and apoptosis. In fact, due to mitochondria involvement in so many crucial cellular processes in metabolic relevant tissues, mitochondrial dysfunction has been linked to different metabolic diseases, including insulin resistance and type 2 diabetes. Herein, we review the main mechanisms whereby metabolism-disrupting chemical (MDC), a subclass of EDCs that disturbs energy homeostasis, cause mitochondrial dysfunction, thus contributing to the establishment of insulin resistance and type 2 diabetes. We conclude that MDC-induced mitochondrial dysfunction, which is mainly characterized by perturbations in mitochondrial bioenergetics, biogenesis, and dynamics, excessive reactive oxygen species production, and activation of the mitochondrial pathway of apoptosis, seems to be a relevant mechanism linking MDCs to type 2 diabetes development.

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Section: Mdcs and Mitochondrial Biogenesismentioning

confidence: 99%

Mitochondria as target of endocrine-disrupting chemicals: implications for type 2 diabetes

Marroquí

Tudurí

Alonso-Magdalena

et al. 2018

Journal of Endocrinology

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“…SIRT3 induces Nrf2 which is responsible for transcription of important antioxidant factors. These antioxidant factors fight against oxidative stress [42][43][44]. SIRT3 elevates SOD2's activity by deacetylation [45].…”

Section: Discussionmentioning

confidence: 99%

Tubeimoside I Ameliorates Myocardial Ischemia‐Reperfusion Injury through SIRT3‐Dependent Regulation of Oxidative Stress and Apoptosis

Luo

Cheng

et al. 2021

Oxidative Medicine and Cellular Longevity

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Myocardial ischemia-reperfusion injury (MIRI) is a phenomenon that reperfusion leads to irreversible damage to the myocardium and increases mortality in acute myocardial infarction (AMI) patients. There is no effective drug to treat MIRI. Tubeimoside I (TBM) is a triterpenoid saponin purified from Chinese traditional medicine tubeimu. In this study, 4 mg/kg TBM was given to mice intraperitoneally at 15 min after ischemia. And TBM treatment improved postischemic cardiac function, decreased infarct size, diminished lactate dehydrogenase release, ameliorated oxidative stress, and reduced apoptotic index. Notably, ischemia-reperfusion induced a significant decrease in cardiac SIRT3 expression and activity, while TBM treatment upregulated SIRT3’s expression and activity. However, the cardioprotective effects of TBM were largely abolished by a SIRT3 inhibitor 3-(1H-1,2,3-triazol-4-yl) pyridine (3-TYP). This suggests that SIRT3 plays an essential role in TBM’s cardioprotective effects. In vitro, TBM also protected H9c2 cells against simulated ischemia/reperfusion (SIR) injury by attenuating oxidative stress and apoptosis, and siSIRT3 diminished its protective effects. Taken together, our results demonstrate for the first time that TBM protects against MIRI through SIRT3-dependent regulation of oxidative stress and apoptosis. TBM might be a potential drug candidate for MIRI treatment.

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“…The transcriptional activity of mPXR and hPXR were also activated up to 6-fold by MBzP [198]. Exposure of 10 nM BBP in HepG2 cells caused downregulation of Sirt1 and Sirt3, which are histone deacetylases acting as cell protecting factors in stress response, PPARγ corepressor and sensors of nutrient/energy levels in the cell [199].…”

Section: Obesity/type 2 Diabetes In Vitro Studiesmentioning

confidence: 97%

New EU criteria for endocrine disrupters

2018

TemaNord

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The plasticizer BBP selectively inhibits epigenetic regulator sirtuins

Cited by 20 publications

References 66 publications

Mitochondria as target of endocrine-disrupting chemicals: implications for type 2 diabetes

Mitochondria as target of endocrine-disrupting chemicals: implications for type 2 diabetes

Tubeimoside I Ameliorates Myocardial Ischemia‐Reperfusion Injury through SIRT3‐Dependent Regulation of Oxidative Stress and Apoptosis

New EU criteria for endocrine disrupters

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