Autophagy as a second level protective process in conferring resistance to environmentally-induced oxidative stress

This conceptual paper addresses the role of lysosomal autophagy in cellular defense against environmentally-induced oxidative stress using a marine mollusc (the blue mussel) as an experimental model. It is proposed that augmented autophagic removal of oxidatively damaged organelles and proteins provides a second level or tier of defense against oxidative stress. Age pigment or lipofuscin is a product of oxidative attack on proteins and lipids and can accumulate in lysosomes, where it may generate further reactive oxygen species (ROS) and inhibit Iysosomal function, resulting in autophagic failure. The previously observed protective role of augmented 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 minimizing formation of potentially harmful stress/age pigment, and has been proposed as an anti-aging mechanism. Finally, the probable low level triggering of autophagy in mussels by fluctuating environmental regimes is considered as a potential protective mechanism that will contribute to resistance to environmentally induced oxidative stress. It is further conjectured that organisms making up functional ecological assemblages (communities) in fluctuating environments, where upregulation of autophagy should provide a selective advantage, may be pre-selected to be tolerant of pollutant-induced oxidative stress.