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damaged organelles, proteins, phospholipids, and lipids contributing to further lipofuscin
formation (Moore 1988; Krishnakumar et al. 1994; Brunk and Terman 2002; Moore et al.
2006a, b, c).
Failed autophagy has been observed in mollusks, fish, and mammals exposed to pol-
lutants (Moore 1988; Allen and Moore 2004; Moore et al. 2004a, 2006a, b, c). Reports on
other animals tend to be largely descriptive, so systematic observations of other phyletic
groups would be beneficial to the development of a generic understanding of the role of
autophagy in ameliorating the harmful effects of pollutants.
5.4.4 Linking Lysosomal and Autophagic Responses to Higher Level Effects
Since autophagy is probably one of the most highly evolutionarily conserved molecular
processes in the eukaryotes (Klionsky and Emr 2000; Cuervo 2004), it is hypothesized that
up-regulation of this system may play a significant role in adaptation to environments
where oxidative stress is a major selection pressure, and where the facility to rapidly delete
and recycle oxidatively damaged proteins and organelles will provide an evolutionary
advantage (Figure 5.4).
Many mollusks have such a capability for augmented autophagy, including mussels and
marine and terrestrial snails (Moore and Halton 1973; Bayne et al. 1978; Lowe et al. 1981;
Moore et al. 1985, 2006a; Pipe and Moore 1986a, b; Moore 2004; Marigómez et al. 2005b).
Augmented autophagy induced by short-term starvation has a protective effect against
copper and phenanthrene-mediated oxidative stress in mussels (Moore 2004; Shaw et al.
2011). Further support comes from a study of blue mussels
Mytilus edulis
from a highly
contaminated site in Norway that showed evidence of tolerance, in comparison with less
contaminated mussels (Figure 5.5; Moore 1988). Samples from four sites along a pollution
gradient showed that lysosomal stability in mussels from the most contaminated site was
more similar to that in mussels from the cleanest site, than their counterparts from inter-
mediate sites. Although these heavily contaminated mussels had relatively high lysosomal
stability, they showed clear evidence of autophagy, placing them in Tier 2, whereas mus-
sels from intermediate sites with low lysosomal stability were clearly in Tier 3 (Figure 5.6;
Moore 1988). The inference here is that up-regulated autophagy may have been selected in
this heavily contaminated population (Moore 1988). Lysosomal stability was also strongly
correlated with macrobenthic diversity (
H
ʹ) in spatially adjacent sites (Figure 5.5;
R
= 0.946,
P
< 0.01), and although these are just correlations, they may be a reflection of the universal-
ity of autophagic reactions to stress.
In addition to studies of single populations and species, many studies have examined
changes in the structure of communities along marine pollution gradients (Gray et al.
1988). Indeed, this is a standard component of most pollution monitoring schemes. One
common finding is that responses are often manifest at taxonomic levels higher than spe-
cies, commonly as high as phyla (Olsgard et al. 1998). Organisms within different phyla
are considered to have different sensitivities to stress (Warwick and Clarke 1993), raising
the interesting possibility that this reflects long-established evolutionary differences in
the physiology of organisms within different phyla. Although autophagic mechanisms are
highly conserved among eukaryotes, we hypothesize that ability to up-regulate this pro-
cess varies among phyla, and this underlies differences in the ability of different animals
to colonize parts of the coastal and estuarine environment and also contributes to their
differential sensitivities to anthopogenic stress. We propose that representative organ-
isms from a range of phyla making up functional ecological assemblages be assessed to
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