Data from: A significant component of ageing (DNA damage) is reflected in fading breeding colors: an experimental test using innate antioxidant mimetics in painted dragon lizards
Olsson, Mats Michael, University of Sydney
Tobler, Michael, University of Sydney
Healey, Mo, University of Sydney
Perrin, Cecile, University of Wollongong
Wilson, Mark, University of Wollongong
Published Feb 21, 2012 on Dryad.
Cite this dataset
Olsson, Mats Michael et al. (2012). Data from: A significant component of ageing (DNA damage) is reflected in fading breeding colors: an experimental test using innate antioxidant mimetics in painted dragon lizards [Dataset]. Dryad. https://doi.org/10.5061/dryad.bb5dr437
A decade ahead of their time, von Schantz and coworkers united sexual selection and free radical biology by identifying causal links between deep-rooted physiological processes that dictate resistance to toxic waste from oxidative metabolism (reactive oxygen species), and phenotypic traits, such as ornaments. Ten years later, these ideas have still only been tested with indirect estimates of free radical levels (oxidative stress) subsequent to the action of innate and dietary antioxidants. Here we measure net superoxide (a selection pressure for antioxidant production) and experimentally manipulate superoxide antioxidation using a synthetic mimetic of superoxide dismutase, Eukarion 134 (EUK). We then measure the toxic effect of superoxide in terms of DNA erosion and concomitant loss of male breeding coloration in the lizard, Ctenophorus pictus. Control males suffered more DNA damage than EUK-males. Spectroradiometry showed that male coloration is lost in relation to superoxide and covaries with DNA erosion; in control males these variables explained 72 % of color loss, whereas in EUK males, the fading of coloration was unaffected by superoxide and unrelated to DNA damage. Thus, EUK’s powerful antioxidation removes the erosion effect of superoxide on coloration and experimentally verifies the prediction that colors reflect innate capacity for antioxidation.