Pyrrolidine Dithiocarbamate (PDTC) Inhibits DON-Induced Mitochondrial Dysfunction and Apoptosis via the NF-κB/iNOS Pathway
Jazyk angličtina Země Spojené státy americké Médium electronic-ecollection
Typ dokumentu časopisecké články
PubMed
30595795
PubMed Central
PMC6286745
DOI
10.1155/2018/1324173
Knihovny.cz E-zdroje
- MeSH
- antioxidancia MeSH
- apoptóza MeSH
- lidé MeSH
- mitochondrie metabolismus MeSH
- NF-kappa B metabolismus MeSH
- oxidační stres MeSH
- pyrrolidiny farmakologie terapeutické užití MeSH
- signální transdukce MeSH
- thiokarbamáty farmakologie terapeutické užití MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- antioxidancia MeSH
- NF-kappa B MeSH
- pyrrolidine dithiocarbamic acid MeSH Prohlížeč
- pyrrolidiny MeSH
- thiokarbamáty MeSH
Oxidative stress is closely linked to the toxic responses of various cell types in normal and pathophysiological conditions. Deoxynivalenol (DON), an inducer of stress responses in the ribosome and the endoplasmic reticulum (ER), causes mitochondrial dysfunction and mitochondria-dependent apoptosis through oxidative stress in humans and animals. The NF-κB pathway, which is closely linked to oxidative stress, is hypothesized to be a critical signaling pathway for DON-induced toxicity and is a potential target for intervention. The present study was conducted to explore the protective effects of pyrrolidine dithiocarbamate (PDTC) from the toxic effects of DON in rat anterior pituitary GH3 cells. Our results showed that DON activated the NF-κB transcription factors and induced cellular oxidative stress, mitochondrial dysfunction, and apoptosis. Morphological studies using transmission electron microscopy (TEM) and cell apoptosis analyses suggested that PDTC prevented DON-induced mitochondrial dysfunction and apoptosis, probably by preventing the DON-induced translocation of NF-κB p65 into the nucleus, and by inhibiting DON-induced iNOS expression. This led to the blocking of the NF-κB pathway and inhibition of iNOS activity.
College of Life Science Yangtze University Jingzhou China
Hubei Collaborative Innovation Center for Animal Nutrition and Feed Safety Wuhan 430070 China
Zobrazit více v PubMed
Bondy G. S., Coady L., Curran I., et al. Effects of chronic deoxynivalenol exposure on p 53 heterozygous and p 53 homozygous mice. Food and Chemical Toxicology. 2016;96:24–34. doi: 10.1016/j.fct.2016.07.018. PubMed DOI
Kosawang C., Karlsson M., Jensen D., Dilokpimol A., Collinge D. B. Transcriptomic profiling to identify genes involved in Fusarium mycotoxin deoxynivalenol and zearalenone tolerance in the mycoparasitic fungus Clonostachys rosea. BMC Genomics. 2014;15(1):p. 55. doi: 10.1186/1471-2164-15-55. PubMed DOI PMC
Pinton P., Oswald I. Effect of deoxynivalenol and other type B trichothecenes on the intestine: a review. Toxins. 2014;6(5):1615–1643. doi: 10.3390/toxins6051615. PubMed DOI PMC
Rocha O., Ansari K., Doohan F. M. Effects of trichothecene mycotoxins on eukaryotic cells: a review. Food Additives and Contaminants. 2005;22(4):369–378. doi: 10.1080/02652030500058403. PubMed DOI
Wu Q., Dohnal V., Huang L., Kuča K., Yuan Z. Metabolic pathways of trichothecenes. Drug Metabolism Reviews. 2010;42(2):250–267. doi: 10.3109/03602530903125807. PubMed DOI
Pestka J. J. Deoxynivalenol-induced proinflammatory gene expression: mechanisms and pathological sequelae. Toxins. 2010;2(6):1300–1317. doi: 10.3390/toxins2061300. PubMed DOI PMC
Shi Y., Porter K., Parameswaran N., Bae H. K., Pestka J. J. Role of GRP 78/BiP degradation and ER stress in deoxynivalenol-induced interleukin-6 upregulation in the macrophage. Toxicological Sciences. 2009;109(2):247–255. doi: 10.1093/toxsci/kfp060. PubMed DOI PMC
Wu Q. H., Wang X., Yang W., et al. Oxidative stress-mediated cytotoxicity and metabolism of T-2 toxin and deoxynivalenol in animals and humans: an update. Archives of Toxicology. 2014;88(7):1309–1326. doi: 10.1007/s00204-014-1280-0. PubMed DOI
Bensassi F., Gallerne C., Sharaf el Dein O., Lemaire C., Hajlaoui M. R., Bacha H. Involvement of mitochondria-mediated apoptosis in deoxynivalenol cytotoxicity. Food and Chemical Toxicology. 2012;50(5):1680–1689. doi: 10.1016/j.fct.2012.01.015. PubMed DOI
Ma Y., Zhang A., Shi Z., et al. A mitochondria-mediated apoptotic pathway induced by deoxynivalenol in human colon cancer cells. Toxicology in Vitro. 2012;26(3):414–420. doi: 10.1016/j.tiv.2012.01.010. PubMed DOI
Wang X., Liu Q., Ihsan A., et al. JAK/STAT pathway plays a critical role in the proinflammatory gene expression and apoptosis of RAW264.7 cells induced by trichothecenes as DON and T-2 toxin. Toxicological Sciences. 2012;127(2):412–424. doi: 10.1093/toxsci/kfs106. PubMed DOI
Tiemann U., Brüssow K. P., Dannenberger D., et al. The effect of feeding a diet naturally contaminated with deoxynivalenol (DON) and zearalenone (ZON) on the spleen and liver of sow and fetus from day 35 to 70 of gestation. Toxicology Letters. 2008;179(3):113–117. doi: 10.1016/j.toxlet.2008.04.016. PubMed DOI
Amuzie C. J., Pestka J. J. Suppression of insulin-like growth factor acid-labile subunit expression—a novel mechanism for deoxynivalenol-induced growth retardation. Toxicological Sciences. 2010;113(2):412–421. doi: 10.1093/toxsci/kfp225. PubMed DOI PMC
Voss K. A. A new perspective on deoxynivalenol and growth suppression. Toxicological Sciences. 2010;113(2):281–283. doi: 10.1093/toxsci/kfp287. PubMed DOI
Wan D., Wang X., Wu Q., et al. Integrated transcriptional and proteomic analysis of growth hormone suppression mediated by trichothecene T-2 toxin in rat GH 3 cells. Toxicological Sciences. 2015;147(2):326–338. doi: 10.1093/toxsci/kfv131. PubMed DOI
Krishnaswamy R., Devaraj S. N., Padma V. V. Lutein protects HT-29 cells against deoxynivalenol-induced oxidative stress and apoptosis: prevention of NF-κB nuclear localization and down regulation of NF-κB and cyclo-oxygenase-2 expression. Free Radical Biology and Medicine. 2010;49(1):50–60. doi: 10.1016/j.freeradbiomed.2010.03.016. PubMed DOI
Van De Walle J., Romier B., Larondelle Y., Schneider Y.-J. Influence of deoxynivalenol on NF-κB activation and IL-8 secretion in human intestinal Caco-2 cells. Toxicology Letters. 2008;177(3):205–214. doi: 10.1016/j.toxlet.2008.01.018. PubMed DOI
Karin M., Ben-Neriah Y. Phosphorylation meets ubiquitination: the control of NF-κB activity. Annual Review of Immunology. 2000;18(1):621–663. doi: 10.1146/annurev.immunol.18.1.621. PubMed DOI
Steinbrecher K. A., Wilson W., Cogswell P. C., Baldwin A. S. Glycogen synthase kinase 3β functions to specify gene-specific, NF-κB-dependent transcription. Molecular and Cellular Biology. 2005;25(19):8444–8455. doi: 10.1128/MCB.25.19.8444-8455.2005. PubMed DOI PMC
Morgan M. J., Liu Z. G. Crosstalk of reactive oxygen species and NF-κB signaling. Cell Research. 2011;21(1):103–115. doi: 10.1038/cr.2010.178. PubMed DOI PMC
Liu X., Guo P., Liu A., et al. Nitric oxide (NO)-mediated mitochondrial damage plays a critical role in T-2 toxin-induced apoptosis and growth hormone deficiency in rat anterior pituitary GH3 cells. Food and Chemical Toxicology. 2017;102:11–23. doi: 10.1016/j.fct.2017.01.017. PubMed DOI
Kowaltowski A. J., Vercesi A. E. Mitochondrial damage induced by conditions of oxidative stress. Free Radical Biology and Medicine. 1999;26(3-4):463–471. doi: 10.1016/S0891-5849(98)00216-0. PubMed DOI
Lee J., Giordano S., Zhang J. Autophagy, mitochondria and oxidative stress: cross-talk and redox signalling. The Biochemical Journal. 2012;441(2):523–540. doi: 10.1042/BJ20111451. PubMed DOI PMC
Zhang X., Jiang L., Geng C., Cao J., Zhong L. The role of oxidative stress in deoxynivalenol-induced DNA damage in HepG2 cells. Toxicon. 2009;54(4):513–518. doi: 10.1016/j.toxicon.2009.05.021. PubMed DOI
Chaudhari M., Jayaraj R., Bhaskar A. S. B., Lakshmana Rao P. V. Oxidative stress induction by T-2 toxin causes DNA damage and triggers apoptosis via caspase pathway in human cervical cancer cells. Toxicology. 2009;262(2):153–161. doi: 10.1016/j.tox.2009.06.002. PubMed DOI
Dvorska J. E., Pappas A. C., Karadas F., Speake B. K., Surai P. F. Protective effect of modified glucomannans and organic selenium against antioxidant depletion in the chicken liver due to T-2 toxin-contaminated feed consumption. Comparative Biochemistry and Physiology Part C: Toxicology & Pharmacology. 2007;145(4):582–587. doi: 10.1016/j.cbpc.2007.02.005. PubMed DOI
Wu J., Tu D., Yuan L. Y., Yuan H., Wen L. X. T-2 toxin exposure induces apoptosis in rat ovarian granulosa cells through oxidative stress. Environmental Toxicology and Pharmacology. 2013;36(2):493–500. doi: 10.1016/j.etap.2013.03.017. PubMed DOI
Buss H., Dörrie A., Schmitz M. L., Hoffmann E., Resch K., Kracht M. Constitutive and interleukin-1-inducible phosphorylation of p65 NF-κB at serine 536 is mediated by multiple protein kinases including IκB kinase (IKK)-α, IKKβ, IKKϵ, TRAF family member-associated (TANK)-binding kinase 1 (TBK1), and an unknown kinase and couples p65 to TATA-binding protein-associated factor II31-mediated interleukin-8 transcription. Journal of Biological Chemistry. 2004;279(53):55633–55643. doi: 10.1074/jbc.m409825200. PubMed DOI
Eberhardt W., Kunz D., Hummel R., Pfeilschifter J. Molecular cloning of the rat inducible nitric oxide synthase gene promoter. Biochemical and Biophysical Research Communications. 1996;223(3):752–756. doi: 10.1006/bbrc.1996.0968. PubMed DOI
Bensassi F., el Golli-Bennour E., Abid-Essefi S., Bouaziz C., Hajlaoui M. R., Bacha H. Pathway of deoxynivalenol-induced apoptosis in human colon carcinoma cells. Toxicology. 2009;264(1-2):104–109. doi: 10.1016/j.tox.2009.07.020. PubMed DOI
Ji G. E., Park S. Y., Wong S. S., Pestka J. J. Modulation of nitric oxide, hydrogen peroxide and cytokine production in a clonal macrophage model by the trichothecene vomitoxin (deoxynivalenol) Toxicology. 1998;125(2-3):203–214. PubMed
Bouaziz C., Martel C., Sharaf el dein O., et al. Fusarial toxin-induced toxicity in cultured cells and in isolated mitochondria involves PTPC-dependent activation of the mitochondrial pathway of apoptosis. Toxicological Sciences. 2009;110(2):363–375. doi: 10.1093/toxsci/kfp117. PubMed DOI
Mariappan N., Elks C. M., Sriramula S., et al. NF-κB-induced oxidative stress contributes to mitochondrial and cardiac dysfunction in type ii diabetes. Cardiovascular Research. 2010;85(3):473–483. doi: 10.1093/cvr/cvp305. PubMed DOI PMC