Data for: Oxidative stress, lysosomal damage and dysfunction of autophagy in molluscan hepatopancreas (digestive gland) induced by chemical contaminants

Published: 24 Oct 2019 | Version 1 | DOI: 10.17632/j4xzv3fcgj.1

Description of this data

Autophagy is a highly conserved evolutionary survival or defence process that enables cells and organisms to survive periods of environmental stress by breaking down cellular organelles and macromolecules in autolysosomes to provide a supply of nutrients for cell maintenance. However, autophagy is also a part of normal cellular physiology that facilitates the turnover of cellular constituents under normal conditions: it can be readily augmented by mild environmental stress; but becomes dysfunctional with severe oxidative stress leading to cellular pathology. The molluscan hepatopancreas or digestive gland provides a versatile and environmentally relevant model to investigate lysosomal autophagy and stress-induced dysfunctional autophagy. This latter process has been implicated in many animal and human disease conditions, including degenerative and neurodegenerative diseases, as well as obesity related conditions. Many environmental pollutants have also been found to induce dysfunctional autophagy in molluscan hepatopancreatic digestive cells, and in this study, the marine blue mussel Mytilus galloprovincialis was exposed for 7 days to: 0.1 µM, 1 µM and 10 µM concentrations of fluoranthene and phenanthrene (PAHs); chlorpyrifos and malathion (organophosphorus compounds); atrazine (triazine herbicide); copper (transition metal) and dodecylbenzene sulphonic acid (LAS, surfactant). The marine snail or periwinkle, Littorina littorea, was also exposed to phenanthrene, chlorpyrifos and copper. Indices of oxidative stress, cell injury and dysfunctional autophagy were measured (i.e., lysosomal membrane stability, protein carbonyls, lipofuscin, and lysosomal accumulation of lipid or lipidosis). Evidence of oxidative stress, based on the elevation of lipofuscin and protein carbonyls, was found for all compounds tested; with chlorpyrifos being the most toxic to both species. Dysfunctional autophagy was induced by all of the compounds tested in both species, except for atrazine in mussels. This failure of normal autophagy was consistently associated with oxidative stress. A conceptual mechanistic model has been developed for dysregulation of autophagy, together with a new diagnostic/prognostic system (Euler logical relationship model) for assessing health status based on lysosomal biomarkers and predicting the pathophysiological outcome.

Experiment data files

This data is associated with the following publication:

Oxidative stress, lysosomal damage and dysfunctional autophagy in molluscan hepatopancreas (digestive gland) induced by chemical contaminants

Published in: Marine Environmental Research

Latest version

  • Version 1


    Published: 2019-10-24

    DOI: 10.17632/j4xzv3fcgj.1

    Cite this dataset

    Moore, Michael N; Al-Moosawi, Lisa; Mou, Zhuofan; Langston, Bill; Frickers, Patricia; Readman, James; Lowe, David; Beesley, Amanda; Pascoe, Christine; Shaw, Jennifer (2019), “Data for: Oxidative stress, lysosomal damage and dysfunction of autophagy in molluscan hepatopancreas (digestive gland) induced by chemical contaminants ”, Mendeley Data, v1


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Environmental Toxicology, Environmental Pathology, Marine Ecotoxicology


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