ZFIN ID: ZDB-PUB-080306-24
Fullerene C(60) exposure elicits an oxidative stress response in embryonic zebrafish
Usenko, C.Y., Harper, S.L., and Tanguay, R.L.
Date: 2008
Source: Toxicol. Appl. Pharmacol. 229(1): 44-55 (Journal)
Registered Authors: Tanguay, Robert L.
Keywords: Fullerene, Photoactivation, Gene expression
MeSH Terms: Acetylcysteine/pharmacology; Animals; Buthionine Sulfoximine/pharmacology; Carrier Proteins/drug effects; Carrier Proteins/metabolism (all 26) expand
PubMed: 18299140 Full text @ Toxicol. Appl. Pharmacol.
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.
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