A meta-analysis of glucocorticoids as modulators of oxidative stress in vertebrates

Abstract

Prolonged high secretion of glucocorticoids normally reflects a state of chronic stress, which has been associated with an increase in disease susceptibility and reduction in Darwinian fitness. Here, we hypothesize that an increase in oxidative stress accounts for the detrimental effects of prolonged high secretion of glucocorticoids. We performed a meta-analysis on studies where physiological stress was induced by administration of glucocorticoids to evaluate the magnitude of their effects on oxidative stress. Glucocorticoids have a significant effect on oxidative stress (Pearson r = 0.552), although this effect depends on the duration of treatment, and is larger in long-term experiments. Importantly, there was a significant effect on tissue, with brain and heart being the most and the least susceptible to GC-induced oxidative stress, respectively. Furthermore, effect size was larger (1) in studies using both sexes compared to males only, (2) when corticosterone rather than dexamethasone was administered and (3) in juveniles than in adults. These effects were not confounded by species, biochemical biomarker, or whether wild or laboratory animals were studied. In conclusion, our meta-analysis suggests that GC-induced oxidative stress could be a further mechanism underlying increases in disease susceptibility and decreases in Darwinian fitness observed under chronic stress.

Family-transmitted stress in a wild bird

“…Living with stressed siblings also resulted in increased level of oxidative damage to lipids and proteins when chicks were near fledging, indicating that stress cross-over was oxidatively costly for gull fledglings. These oxidative costs support the general view of glucocorticoid hormones as modulators of oxidative status in vertebrates (22). In birds, prenatal elevation of corticosterone levels is associated with postnatal oxidative costs (40), agreeing with our result of the longterm effect of early exposure to corticosterone on oxidative damage.…”

“…Despite the possible benefits of stress cross-over, a protracted stress exposure can be damaging (16,17), particularly when occurring during early stages of development (18)(19)(20). Early exposure to stressful conditions can, for instance, negatively affect growth rates (11,16), the development of key body structures [i.e., feathers in birds (21)], and promote the accumulation of oxidative damage (22). To fully understand the role of stress cross-over in animal populations, it is fundamental to assess the costs and benefits, if any, of such phenomena.…”

Physiological Stress Responses in Amphibian Larvae to Multiple Stressors Reveal Marked Anthropogenic Effects even below Lethal Levels

“…Elevated GCs cause an increased metabolic rate involving overproduction of reactive oxygen species (ROS; Peckett et al 2011) that often results in cellular damage (Circu and Aw 2010). Such cellular damage, however, can be buffered by increasing the activity of antioxidant enzymes (Costantini et al 2011;Gomez-Mestre et al 2013). Additionally, GCs are inmmunomodulators that can exert both negative and positive effects on the immune status of individuals (Franchimont 2004), depending on the duration and intensity of the exposure to stress (Rich and Romero 2005), although chronic exposure to high GC levels seems associated with immune deregulation (Padgett and Glaser 2003).…”

Kesan Psikostres terhadap Kerosakan DNA dan Ketaknormalan Titisan Sitoplasma Sperma Manusia

“…Cetusan ini mempunyai hubungan dengan alostosis. Walau bagaimanapun, kegagalan alostosis mengaruh pengumpulan hormon glukokortikoid secara berlebihan dan lama-kelamaan akan mewujudkan spesies oksigen reaktif (ROS) (Constantini et al 2011). Pada tahap minimal, ROS adalah baik untuk sperma, namun apabila ROS wujud secara berlebihan ia akan memberi kesan stres oksidatif dan keadaan ini akan mengancam kenormalan sperma dan seterusnya mencederakan struktur DNA (Chen et al 2012).…”