In this study, we used an integrated approach to determine whether key biochemical, cellular, and physiological responses were related to growth impairment of cadmium (Cd)-exposed larval topsmelt (Atherinops affinis). Food intake (Artemia franciscana nauplii), oxygen consumption rates, apoptotic DNA fragmentation (TUNEL assay), and metallothionein (MT)-like protein levels, were separately measured in relation to growth of larval topsmelt aqueously exposed to sublethal doses of Cd for 14 days. Cadmium accumulation and concentrations of abundant metals were also evaluated in a subset of fish. Fish in the highest Cd treatments (50 and 100 ppb Cd) were smaller in final mean weight and length, and consumed fewer A. franciscana nauplii than control fish. Food intake was positively correlated with final weight of larval topsmelt in Cd and control treatments; food intake increased as final weight of the fish increased. Oxygen consumption rates were positively correlated with Cd concentration and mean oxygen consumption rates were inversely correlated with final mean weight of topsmelt; the smallest fish were found in the highest Cd treatment and were respiring at higher rates than control fish. Apoptotic DNA fragmentation was concentration-dependent and was associated with diminished growth. Apoptotic DNA fragmentation was elevated in the gill of fish exposed to 50 ppb Cd, and in the gut, gill, and liver of fish exposed to 100 ppb Cd. Metallothionein (MT)-like protein levels in fish from 100 ppb Cd treatments were significantly higher than those in other treatments. Oxygen consumption rates may have increased as a compensatory response to Cd exposure. However, it is likely that the energy produced was allocated to an increased metabolic demand due to apoptosis, MT synthesis, and changes in ion regulation. This diversion of energy expenditures could contribute to growth impairment of Cd-exposed fish.
|Number of pages||11|
|State||Published - Dec 1 2006|
Bibliographical noteFunding Information:
This research has been supported by a grant from the US Environmental Protection Agency's Science to Achieve Results (STAR) Estuarine and Great Lakes (EaGLe) program through funding to the Pacific Estuarine Ecosystem Indicator Research (PEEIR) Consortium, US EPA Agreement #R-882867601. The research described in this article has not been subjected to any EPA review and therefore does not necessarily reflect the views of the Agency, and no official endorsement should be inferred. We thank the UC Davis Jastro-Shields Graduate Research Award and the Ecotoxicology and Coastal Toxicology components of the UC Toxic Substances Research and Teaching Program for additional financial support. We also thank Ellie Fairbairn, Sheila Walsh, Carol Vines, Allison Briden, and Kevin Hovel.
- Physiological responses
ASJC Scopus subject areas
- Aquatic Science
- Health, Toxicology and Mutagenesis