This conceptual paper addresses the role of lysosomal autophagy in cellular defence against oxidative stress. A hypothesis is proposed that autophagic removal of oxidatively damaged organelles and proteins provides a second tier of defence against oxidative stress. Age pigment or lipofuscin is a product of oxidative attack on proteins and lipids and can accumulate in lysosomes, where it can generate reactive oxygen species (ROS) and inhibit lysosomal function, resulting in autophagic failure. It is further hypothesised that repeated triggering of augmented autophagy can protectively minimise lipofuscin generation; and that animals living in fluctuating environments, where autophagy is repeatedly stimulated by natural stressors, will be generically more tolerant of pollutant stress. Data for resistance to pollutant stress is presented, together with evidence for a correlation between lysosomal stability and macrobenthic diversity. Finally, we speculate that organisms making up functional ecological assemblages in fluctuating environments, where up-regulation of autophagy should provide a selective advantage, may be pre-selected to be tolerant of pollutant-induced oxidative stress.