|Autophagic and lysosomal reactions to stress in the hepatopancreas of blue mussels|Moore, M.N.; Viarengo, A.; Donkin, P.; Hawkins, A.J.S. (2007). Autophagic and lysosomal reactions to stress in the hepatopancreas of blue mussels. Aquat. Toxicol. 84(1): 80-91. dx.doi.org/10.1016/j.aquatox.2007.06.007
In: Aquatic Toxicology. Elsevier Science: Tokyo; New York; London; Amsterdam. ISSN 0166-445X, more
Lipofuscin; Lysosomes; Pollutants; Tolerance; Mytilus edulis Linnaeus, 1758 [WoRMS]; ANE, British Isles, England, Devon, Exe Estuary [Marine Regions]; Marine
|Authors|| || Top |
- Moore, M.N.
- Viarengo, A.
- Donkin, P.
- Hawkins, A.J.S.
The aim of this investigation was to test the reactions of the hepatopancreatic digestive cells of blue mussels (Mytilus edulis and Mytilus galloprovincialis) to a variety of environmental stressors. These stressors included anoxia, hyperthermia, polycyclic aromatic hydrocarbons, copper and a combination of copper + nutritional deprivation. Paraquat was used as an experimental generator of reactive oxygen species (ROS). All of these stressors induced adverse reactions in the lysosomal system of the digestive cells and many also induced autophagy. Changes induced by anoxia and hyperthermia were reversible, whereas autophagic reactions caused by PAHs were incomplete resulting in swelling and accumulation of lipid and phospholipid in the autolysosomes. The lysosomotropic drug chloroquine, an inducer of incomplete autophagy, enhanced the toxicity of phenanthrene but was not itself toxic at the experimental concentration used. Nutritional deprivation-induced autophagy had a protective effect on lysosomal stability in mussels exposed to copper. These findings complement previous findings and support a mechanistic model for lysosomal responses to free radicals and reactive oxygen (ROS, reactive oxygen species) which are generated by normal metabolism and often enhanced by stress and toxic xenobiotics and metals. The protective role of autophagy induced by nutritional deprivation against oxidative stress can be explained by this model, where autophagy boosts "cellular housekeeping" through enhanced removal of ROS-damaged proteins and organelles minimising formation of harmful stress/age pigment (lipofuscin). Finally, we discuss the possibility of low level triggering of autophagy in mussels by fluctuating environmental regimes providing a mechanism for tolerence to environmental stress.