Meeting Abstract
While there is growing evidence that demographic senescence is an important feature of wild populations, there remains little consensus about any physiological mechanisms that contribute to senescence in wild animals. In birds, many systems appear to remain constant with increasing age, showing no deterioration until ‘catastrophic’ mortality sets in. Oxidative stress may be an important contributor to physiological senescence in wild birds because of their inherently high whole-organism metabolic rate. As a by-product of aerobic respiration, ROS (reactive oxygen species) are produced and can cause structural damage to proteins, lipids and DNA. The anti-oxidant system exists in animals to deter from rapid rates of ROS-related damage to macromolecules. As individuals age, they may accumulate oxidative damage that leads to tissue deterioration. Oxidative stress has been a debated mechanism for aging by gerontologists, ecologists and physiologists. We examined oxidative stress measurements in thick-billed murres by assessing levels of catalase (CAT), glutathione peroxidase (GPx) and superoxide dismutase (SOD) activities, and total antioxidant capacity with respect to peroxyl and hydroxyl scavenging capacity. Additionally, we measured lipid peroxidation (LPO) damage in pectoralis muscle biopsies from wild thick-billed murres aged 8 to 37 years of age (N = 41). When considered in a general linear model with body mass, body size and sex, no parameter varied with age. CAT activity increased with body size while SOD activity was higher in females. Hydroxyl scavenging capacity increased with body mass and decreased with body size. LPO damage, GPx activity and peroxyl scavenging capacity were independent of all parameters. We concluded that muscle oxidative stress levels do not vary with age in thick-billed murres, supporting the catastrophic mortality hypothesis.
