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. 2019 Nov 4;9:15876. doi: 10.1038/s41598-019-52456-3

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Molecular pathway linked to oxidative stress response in E. granulosus PSCs. Exposure to H₂O₂ and other ROS/RNS can cause macromolecule oxidation at the tegumental surface of PSC leading to reactive carbonyls production. Expression of GST at the parasite surface can contribute with the detoxification of some toxic aldehydes (i.e., trans-2-nonenal). Other carbonyl detoxifying enzymes (AKRs, CBRs, and GSTs) are up-regulated to prevent lipid, protein, and DNA damage. Protein modification can cause protein aggregation that can be inhibited by Hsp70 chaperone or degraded by targeting ubiquitinated proteins to 26S proteasome (ADRM1, PSMD2, UCH-L3, and 26S ATP). Damaged mitochondrial membrane and nuclear/mitochondrial DNA could be responsible for initial events of apoptosis, inducing caspase-3 activation and cleavage of protein substrates such as filamins and lamins. ER stress induced by oxidative stress can also be associated with PSC apoptosis. Glycerol production can protect cells from hyperosmotic and oxidative stress. EV: extracellular vesicle, Cytc: cytochrome c, CatD: cathepsin D, Cnx: calnexin, PDI: protein disulfide isomerase.