Toxicity of dyes to zebrafish at the biochemical level: Cellular energy allocation and neurotoxicity.

Abstract

Dyes are widely distributed worldwide, and can be found in wastewaters resulting from industrial or urban effluents. Dyes are of particular concern as contaminants of the aquatic environment, since their toxicity remain poorly understood. Thus, the current study was designed to assess the effects induced by the synthetic azo dye Basic Red 51 (BR51) and by the natural naphthoquinone dye erythrostominone (ERY) on zebrafish early life stages (Danio rerio) at different biological organization levels, i.e., studying how changes in biochemical parameters of important physiological functions (neurotransmission and cellular energy allocation) may be associated with behavior alterations (swimming activity). This approach was also used to assess the effects of ERY after its photodegradation resulting in a colorless product(s) (DERY). Results showed that after 96 h exposure to BR51 and Ery, zebrafish embryos consumed less energy (LOEC = 7.5 mg/L), despite the unaltered levels of available energy (carbohydrates, lipids and proteins). Hence, cellular energy allocation (CEA) was significantly increased. On the other hand, only ERY decreased the acetylcholinesterase activity (LOEC = 15 mg/L). Despite that, zebrafish larvae exposed to both dyes until 144 h were less active. In contrast, DERY did not affect any parameter measured. These results indicate an association between a decrease consumption of energy and decrease swimming activity resulting from an environmental stress condition, independently of the neurotoxicity of the dyes. Degradation of ERY by light prevented all toxic effects previously observed, suggesting a cheap, fast and easy alternative treatment of effluents containing this natural dye. All tools assessed in our current study were sensitive as early-warning endpoints of dyes toxicity on zebrafish early life stages, and suggest that the CEA assay might be useful to predict effects on locomotor activity when cholinergic damage is absent.