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Int. J. Mol. Sci. 2019, 20(8), 1862; https://doi.org/10.3390/ijms20081862

An In Vitro Study on Mitochondrial Compensatory Response Induced by Gliadin Peptides in Caco-2 Cells

1
Laboratory of Nutritional Pathophysiology, National Institute of Gastroenterology “S. de Bellis”, Research Hospital, 70013 Castellana Grotte (Bari), Italy
2
Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari Aldo Moro, Via Orabona 4, 70100 Bari, Italy
*
Author to whom correspondence should be addressed.
These authors equally contributed.
Received: 13 March 2019 / Revised: 10 April 2019 / Accepted: 11 April 2019 / Published: 15 April 2019
(This article belongs to the Special Issue mtDNA and Mitochondrial Stress Signaling in Human Diseases)
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Abstract

Dietary gliadin may show a broad spectrum of toxicity. The interplay between mitochondria and gliadin-induced oxidative stress has not been thoroughly examined in the intestinal epithelium. In this kinetic study, Caco-2 cells were exposed for 24 h to pepsin-trypsin-digested gliadin, alone or in combination with the antioxidant 2,6-di-tbutyl-p-cresol (BHT), and the effects on mitochondrial biogenesis and mtDNA were studied. Cells ability to recover from stress was determined after 24 h and 48 h of incubation in the culture medium. Gliadin-induced oxidative stress evoked a compensatory response. The stressor triggered a rapid and significant increase of Peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) and Peroxiredoxin III (PrxIII) proteins, and mtDNA amount. As for the effects of gliadin on mtDNA integrity, strand breaks, abasic sites, and modified bases were analyzed in three mtDNA regions. D-loop appeared a more fragile target than Ori-L and ND1/ND2. The temporal trend of the damage at D-loop paralleled that of the amount of mtDNA. Overall, a trend toward control values was shown 48 h after gliadin exposure. Finally, BHT was able to counteract the effects of gliadin. Results from this study highlighted the effects of gliadin-induced oxidative stress on mitochondria, providing valuable evidence that might improve the knowledge of the pathophysiology of gluten-related disorders.
Keywords: Caco-2 cells; gliadin; gluten-related disorders; mitochondrial biogenesis; mtDNA; mtDNA damage; oxidative stress; PGC-1α; PrxIII. Caco-2 cells; gliadin; gluten-related disorders; mitochondrial biogenesis; mtDNA; mtDNA damage; oxidative stress; PGC-1α; PrxIII.
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Orlando, A.; Chimienti, G.; Pesce, V.; Fracasso, F.; Lezza, A.M.S.; Russo, F. An In Vitro Study on Mitochondrial Compensatory Response Induced by Gliadin Peptides in Caco-2 Cells. Int. J. Mol. Sci. 2019, 20, 1862.

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