4.5 Article

Are the adverse effects of stressors on amphibians mediated by their effects on stress hormones?

期刊

OECOLOGIA
卷 186, 期 2, 页码 393-404

出版社

SPRINGER
DOI: 10.1007/s00442-017-4020-3

关键词

Atrazine; Batrachochytrium dendrobatidis; Chytrid; Contaminants; Pathogen

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资金

  1. REP Grant from Texas State University
  2. National Science Foundation [EF-1241889]
  3. National Institutes of Health [R01GM109499, R01TW010286]
  4. US Department of Agriculture [NRI 2006-01370, 2009-35102-0543]
  5. US Environmental Protection Agency [CAREER 83518801]
  6. Division Of Environmental Biology
  7. Direct For Biological Sciences [1241889] Funding Source: National Science Foundation

向作者/读者索取更多资源

Adverse effects of anthropogenic changes on biodiversity might be mediated by their impacts on the stress response of organisms. To test this hypothesis, we crossed exposure to metyrapone, a synthesis inhibitor of the stress hormone corticosterone, with exposure to the herbicide atrazine and the fungal pathogen Batrachochytrium dendrobatidis (Bd) to assess whether the effects of these stressors on tadpoles and post-metamorphic frogs were mediated by corticosterone. Metyrapone countered atrazine- and Bd-induced corticosterone elevations. However, atrazine- and Bd-induced reductions in body size were not mediated by corticosterone because they persisted despite metyrapone exposure. Atrazine lowered Bd abundance without metyrapone but increased Bd abundance with metyrapone for tadpoles and frogs. In contrast, atrazine reduced tolerance of Bd infections because frogs exposed to atrazine as tadpoles had reduced growth with Bd compared to solvent controls; this effect was not countered by metyrapone. Our results suggest that the adverse effects of atrazine and Bd on amphibian growth, development, and tolerance of infection are not mediated primarily by corticosterone. A possible mechanism for these effects is energy lost from atrazine detoxification, defense against Bd, or repair from damage caused by atrazine and Bd. Additional studies are needed to evaluate how often the effects of anthropogenic stressors are mediated by stress hormones.

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