However, when I corrected my values of t12 hepatic AP for DNA content, fast-growing AL

turtles had higher AP per cell than both slow-growing R turtles and fast-growing R-AL turtles.

As a result, turtles that underwent an earlier period of CG had decreased cellular antioxidant

function compared to age-matched AL turtles feeding and growing at the same rate. Because I

did not measure hepatic DNA concentration for t5 turtles, I could not evaluate putative AP

content per cell for these individuals.

 The results of this study imply that individuals typically grow at rates that optimize their

ability to prevent oxidative damage to lipids, nucleic acids, and proteins. Oxidative stress results

from an imbalance between the rate of ROS production and the availability of antioxidants to

scavenge these ROS within a cell (Agarwal et al. 2005). Given the assumption that ROS

production increases with intake rate (L6pez-Torres et al. 2002, Barja 2004), my finding that ad

libitum-fed turtles compensating for a prior food restriction also had diminished antioxidant

function implies a cost of CG. It is unclear whether elevated oxidative stress during early

development in this long-lived species would adversely affect longevity or performance.

However, this study provides evidence of cellular stresses coincident with growth compensation

and suggests that sub-maximal growth protects individuals from the detrimental effects of

impaired antioxidant defense.