PUBLICATION
Fullerene C(60) exposure elicits an oxidative stress response in embryonic zebrafish
- Authors
- Usenko, C.Y., Harper, S.L., and Tanguay, R.L.
- ID
- ZDB-PUB-080306-24
- Date
- 2008
- Source
- Toxicology and applied pharmacology 229(1): 44-55 (Journal)
- Registered Authors
- Tanguay, Robyn L.
- Keywords
- Fullerene, Photoactivation, Gene expression
- MeSH Terms
-
- Acetylcysteine/pharmacology
- Animals
- Buthionine Sulfoximine/pharmacology
- Carrier Proteins/drug effects
- Carrier Proteins/metabolism
- Embryo, Nonmammalian/drug effects
- Embryo, Nonmammalian/metabolism
- Ferritins/drug effects
- Ferritins/metabolism
- Fullerenes/toxicity*
- Gene Expression Regulation/drug effects*
- Glutamate-Cysteine Ligase/drug effects
- Glutamate-Cysteine Ligase/metabolism
- Glutathione Transferase/drug effects
- Glutathione Transferase/metabolism
- HSP70 Heat-Shock Proteins/drug effects
- HSP70 Heat-Shock Proteins/metabolism
- Hydrogen Peroxide/metabolism
- Light
- Maleates/pharmacology
- Microarray Analysis
- Models, Animal
- Oxidative Stress/drug effects*
- Pericardial Effusion/chemically induced
- Time Factors
- Zebrafish
- PubMed
- 18299140 Full text @ Tox. App. Pharmacol.
Citation
Usenko, C.Y., Harper, S.L., and Tanguay, R.L. (2008) Fullerene C(60) exposure elicits an oxidative stress response in embryonic zebrafish. Toxicology and applied pharmacology. 229(1):44-55.
Abstract
Due to its unique physicochemical and optical properties, C(60) has raised interest in commercialization for a variety of products. While several reports have determined this nanomaterial to act as a powerful antioxidant, many other studies have demonstrated a strong oxidative potential through photoactivation. To directly address the oxidative potential of C(60), the effects of light and chemical supplementation and depletion of glutathione (GSH) on C(60)-induced toxicity were evaluated. Embryonic zebrafish were used as a model organism to examine the potential of C(60) to elicit oxidative stress responses. Reduced light during C(60) exposure significantly decreased mortality and the incidence of fin malformations and pericardial edema at 200 and 300 ppb C(60). Embryos co-exposed to the glutathione precursor, N-acetylcysteine (NAC), also showed reduced mortality and pericardial edema; however, fin malformations were not reduced. Conversely, co-exposure to the GSH synthesis inhibitors, buthionine sulfoximine (BSO) and diethyl maleate (DEM), increased the sensitivity of zebrafish to C(60) exposure. Co-exposure of C(60) or its hydroxylated derivative, C(60)(OH)(24), with H(2)O(2) resulted in increased mortality along the concentration gradient of H(2)O(2) for both materials. Microarrays were used to examine the effects of C(60) on the global gene expression at two time points, 36 and 48 h post fertilization (hpf). At both life stages there were alterations in the expression of several key stress response genes including glutathione-S-transferase, glutamate cysteine ligase, ferritin, alpha-tocopherol transport protein and heat shock protein 70. These results support the hypothesis that C(60) induces oxidative stress in this model system.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping