期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 108, 期 17, 页码 7086-7090出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1019031108
关键词
cardiac toxicity; fish populations; heart development; oil spills
资金
- National Oceanic and Atmospheric Administration (NOAA)
- Oceans and Human Health Initiative
- California Department of Fish and Game's Oil Spill Response Trust
- Oiled Wildlife Care Network, School of Veterinary Medicine, University of California, Davis
- NOAA Office of Sea [NA 16RG2321, R/97-01]
- University of Alaska
Exposure to high concentrations of crude oil produces a lethal syndrome of heart failure in fish embryos. Mortality is caused by cardiotoxic polycyclic aromatic hydrocarbons (PAHs), ubiquitous components of petroleum. Here, we show that transient embryonic exposure to very low concentrations of oil causes toxicity that is sublethal, delayed, and not counteracted by the protective effects of cytochrome P450 induction. Nearly a year after embryonic oil exposure, adult zebrafish showed subtle changes in heart shape and a significant reduction in swimming performance, indicative of reduced cardiac output. These delayed physiological impacts on cardiovascular performance at later life stages provide a potential mechanism linking reduced individual survival to population-level ecosystem responses of fish species to chronic, low-level oil pollution.
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