Intraspecific support for the climate variability hypothesis: oxidative damage in lizards after acute temperature exposure.

Ectotherms face mounting challenges from climate variability. The climate variability hypothesis predicts that species from more variable environments will exhibit greater physiological resilience, but this has been largely untested within a species. Because ectotherm metabolic rates increase with temperature, mitochondrial function and its byproduct, reactive oxygen species, may play key roles in this thermal resilience. This study examined how temperature affects oxidative damage in prairie lizards (Sceloporus consobrinus) from three populations (northern, central and southern) along a latitudinal gradient in two separate experiments on different individuals. In the first experiment, lizards were exposed to day-long thermal exposures (18°C and 37°C). Oxidative damage, measured as 8-hydroxy-2'-deoxyguanosine (8-OHdG), increased in only the central and southern populations after cold exposure. Notably, the northern population, consistent with predictions of the climate variability hypothesis, showed no increase, suggesting possible adaptations to mitigate cold-induced oxidative damage. In the second experiment, we tested whether oxidative damage was triggered by cold exposure or subsequent rewarming. Again, northern lizards showed no change, whereas southern lizards increased damage with faster rewarming rates. Finally, we found that 8-OHdG decreased 24-h after the cold exposure and rewarming, indicating it may be reversible. Collectively, these results provide the first intraspecific evidence for the climate variability hypothesis in a vertebrate ectotherm. This suggests that cold-adapted lizards possess mechanisms to buffer oxidative damage, emphasizing the role of mitochondrial function and oxidative resilience in shaping thermal tolerances.