DNA damage as an indicator of chronic stress: Correlations with corticosterone and uric acid

Abstract

Corticosterone does not change in consistent ways across species and contexts, making it challenging to use as an indicator of chronic stress. We assessed DNA damage as a potential metric that could be a more integrative stress measurement with direct links to health. We captured free-living house sparrows, took an immediate blood sample, and transferred them to the laboratory, exposing them to the chronic stress of captivity. Biweekly blood and weight samples were then taken for 4 weeks. We immediately assessed DNA damage in red blood cells using the comet assay and later quantified corticosterone. Uric acid was analyzed in a separate group of birds. We found that birds initially lost, but began to regain weight over the course of captivity. DNA damage peaked within the first 10 days of captivity, and mostly remained elevated. However, the cellular distribution of damage changed considerably over time; most cells showed low levels of damage early, a bimodal distribution of high and low DNA damage during the peak of damage, and a wide unimodal distribution of damage at the end of the 4 weeks. Furthermore, corticosterone increased and remained elevated and uric acid decreased and remained depleted over the same period. Although both a molecular (DNA damage) and an endocrine (corticosterone) marker showed similar response profiles over the 4 weeks, they were not correlated, suggesting they reflect different aspects of the underlying physiology. These data provide convincing preliminary evidence that DNA damage has potential to be an additional indicator of chronic stress.