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Arctica islandica; Bivalves; Comparative biology; Endoplasmic reticulum stress; Longevity; Oxidation; Stress resistance
Abstract:
Bivalve molluscs are newly discovered models of successful aging. Here, we test the hypothesis that extremely long-lived
bivalves are not uniquely resistant to oxidative stressors (eg, tert-butyl hydroperoxide, as demonstrated in previous studies)
but exhibit a multistress resistance phenotype. We contrasted resistance (in terms of organismal mortality) to genotoxic
stresses (including topoisomerase inhibitors, agents that cross-link DNA or impair genomic integrity through DNA
alkylation or methylation) and to mitochondrial oxidative stressors in three bivalve mollusc species with dramatically
differing life spans: Arctica islandica (ocean quahog), Mercenaria mercenaria (northern quahog), and the Atlantic bay
scallop, Argopecten irradians irradians (maximum species life spans: >500, >100, and ~2 years, respectively). With all
stressors, the short-lived A i irradians were significantly less resistant than the two longer lived species. Arctica islandica
were consistently more resistant than M mercenaria to mortality induced by oxidative stressors as well as DNA methylating
agent nitrogen mustard and the DNA alkylating agent methyl methanesulfonate. The same trend was not observed for
genotoxic agents that act through cross-linking DNA. In contrast, M mercenaria tended to be more resistant to epirubicin
and genotoxic stressors, which cause DNA damage by inhibiting topoisomerases. To our knowledge, this is the first study
comparing resistance to genotoxic stressors in bivalve mollusc species with disparate longevities. In line with previous
studies of comparative stress resistance and longevity, our data extends, at least in part, the evidence for the hypothesis
that an association exists between longevity and a general resistance to multiplex stressors, not solely oxidative stress.
This work also provides justification for further investigation into the interspecies differences in stress response signatures
induced by a diverse array of stressors in short-lived and long-lived bivalves, including pharmacological agents that
elicit endoplasmic reticulum stress and cellular stress caused by activation of innate immunity.
