2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces oxidative stress, DNA strand breaks, and poly(ADP-ribose) polymerase-1 activation in human breast carcinoma cell lines

Lin, Po-Hsiung; Lin, Chia‐Hua; Huang, Chuan-Chen; Chuang, Ming-Chien; Lin, Pinpin

doi:10.1016/j.toxlet.2007.06.003

Cited by 87 publications

(65 citation statements)

References 59 publications

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“…However, similar differences between MDA-MB-231 and MCF7 cells in response to prooxidants have been observed in previous studies. For example, the pro-oxidant (tert-butyl-2(4,5-dihydrogen-4,4,5,5-tetramethyl-3-O-1H-imidazole-3-cationic-1-oxyl-2-pyrrolidine-1-carboxylic ester) L-NNP induced higher levels of ROS and apoptosis in MDA-MB-231 cells compared to MCF7 cells (Zhang et al 2011) and 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces greater levels of GSH depletion and increased ROS in MDA-MB-231 cells compared to MCF7 cells (Lin et al 2007). Oncogenic transformation has been shown to elevate intracellular ROS (Trachootham et al 2006) or to promote NRF2-dependent ROS detoxification (DeNicola et al 2011), possibly dependent on the level of oncogene expression and or cell type.…”

Section: Discussionmentioning

confidence: 99%

Differential induction of apoptosis in human breast cancer cell lines by phenethyl isothiocyanate, a glutathione depleting agent

Alwi

Cavell

Donlevy

et al. 2012

Cell Stress and Chaperones

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Phenethyl isothiocyanate (PEITC) is a naturally occurring electrophile which depletes intracellular glutathione (GSH) levels and triggers accumulation of reactive oxygen species (ROS). PEITC is of considerable interest as a potential chemopreventive/chemotherapeutic agent, and in this work, we have investigated the effects of PEITC on human breast cancer cell lines. Whereas PEITC readily induced apoptosis in MDA-MB-231 cells (associated with rapid activation of caspases 9 and 3, and decreased expression of BAX), MCF7 cells were relatively resistant to the apoptosis promoting effects of PEITC. The relative resistance of MCF7 cells was associated with high basal expression of NRF2, a transcription factor that coordinates cellular protective responses to oxidants and electrophiles and raised intracellular levels of GSH. This raised basal expression of NRF2 appeared to be a response to on-going production of ROS, since treatment with the antioxidant and GSH precursor N-acetylcysteine (NAC) reduced NRF2 expression. Moreover, pre-treatment of MDA-MB-231 cells with NAC rendered these cells relatively resistant to PEITC-induced apoptosis. In summary, our data confirm that PEITC may be an effective chemopreventive/therapeutic agents for breast cancer. However, differences in the basal expression of NRF2 and resultant changes in GSH levels may be an important determinant of sensitivity to PEITC-induced apoptosis.

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Section: Discussionmentioning

confidence: 99%

Differential induction of apoptosis in human breast cancer cell lines by phenethyl isothiocyanate, a glutathione depleting agent

Alwi

Cavell

Donlevy

et al. 2012

Cell Stress and Chaperones

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“…TCDD activated (liganded) AhR increases the binding of the RelA/p50 complex to the IL-6 promoter. It is believed that TCDD increases NFkB activity by generating reactive oxygen species (Dhar et al, 2002;Lin et al, 2007). On the other hand, unliganded AhR associates with RelA without involving p50 and then binds to the NFkB site of the IL-6 promoter.…”

Section: Discussionmentioning

confidence: 99%

Aryl hydrocarbon receptor in association with RelA modulates IL-6 expression in non-smoking lung cancer

Chang

et al. 2011

Oncogene

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“…ROS produced in high fluxes were demonstrated to cause oxidation of amino acids and to generate PCC products, markers of protein oxidative injury. Studies by Lin et al (2007) have demonstrated that TCDD increased PCC level in the mitochondria of rat hepatocytes. Administration of TCDD along with OO, HT, and TY neutralized the effect of TCDD by reducing LPO (p50.05) and PCC (p50.05) level compared with the TCDD group.…”

Section: Attenuation Of Tcdd-induced Macromolecular Damages By Oo Htmentioning

confidence: 99%

Olive oil and its phenolic compounds (hydroxytyrosol and tyrosol) ameliorated TCDD-induced heptotoxicity in rats via inhibition of oxidative stress and apoptosis

Kalaiselvan

Muniasamy

Archunan

et al. 2015

Pharmaceutical Biology

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Context: Naturally occurring polyphenols including olive oil (OO) and its constituents hydroxytyrosol (HT) and tyrosol (TY), consumed in the Mediterranean diet, have shown to treat various ailments due to their remarkable antioxidant properties. Objective: The present study investigates the hepatoprotective effects of OO and its phenolic compounds HT and TY against TCDD-induced hepatotoxicity in male Wistar rats. Materials and methods: TCDD was administered at a dose of 100 ng/kg p.o. for 20 d. Administration of OO (10 ml/kg; oral), HT (0.5 mg/kg; oral), and TY (30 mg/kg; i.p) was started 5 d prior to TCDD administration, and continued for 25 d with or without TCDD administration. At the end of the experiment (25 d), blood was taken for biochemical analyses and liver for the measurement of macromolecular damages, antioxidant status, expressions of CYP1A1, and apoptotic factors. Results: TCDD administration resulted in significant (p50.05) increase in the level of hepatic stress markers ALT (101.6 ± 3.07 IU/l), AST (295.0 ± 3.0 IU/l), and ALP (266.66 ± 3.7 IU/l). Also, biochemical analyses of liver reported elevation in nitrite and protein carbonyl content and depletion of NQO1 and HO. However, OO, HT, and TY restored the antioxidant status. Protein expressions by Western Blot technique showed an increase in the level of CYP1A1 and Bax and a decreased level of Bcl-2 on TCDD treatment, and vice versa on OO, HT, and TY treatment. Discussion and conclusion: Our work concludes that dietary supplementation of OO, HT, and TY could serve as a potential preventive drug for TCDD-induced hepatotoxicity.

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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces oxidative stress, DNA strand breaks, and poly(ADP-ribose) polymerase-1 activation in human breast carcinoma cell lines

Cited by 87 publications

References 59 publications

Differential induction of apoptosis in human breast cancer cell lines by phenethyl isothiocyanate, a glutathione depleting agent

Differential induction of apoptosis in human breast cancer cell lines by phenethyl isothiocyanate, a glutathione depleting agent

Aryl hydrocarbon receptor in association with RelA modulates IL-6 expression in non-smoking lung cancer

Olive oil and its phenolic compounds (hydroxytyrosol and tyrosol) ameliorated TCDD-induced heptotoxicity in rats via inhibition of oxidative stress and apoptosis

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