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Olaquindox (OLA) has been widely used as an animal feed additive in China for decades; however, its toxicity and toxic mechanisms have not been well investigated. In this study, the developmental neurotoxicity and toxic mechanisms of OLA were evaluated in zebrafish. Zebrafish embryos were exposed to different concentrations of OLA (25-1,000 mg/L) from 6 to 120 hours post fertilization (hpf). OLA exposure resulted in many abnormal phenotypes in zebrafish, including shortened body length, notochord degeneration, spinal curvature, brain apoptosis, damage of axon and peripheral motor neuron, and hepatotoxicity. Interestingly, OLA increased zebrafish spontaneous tail coiling, while reduced locomotor capacity. Quantitative polymerase chain reaction (Q-PCR) showed that the expression levels of nine marker genes for nervous system functions or development, namely, α1-tubulin, glial fibrillary acidic protein (gfap), myelin basic protein (mbp), synapsinII a (syn2a), sonic hedgehog a (shha), encoding HuC (elavl3), mesencephalic astrocyte-derived neurotrophic factor (manf) growth associated protein 43 (gap43), and acetylcholinesterase (ache) were all down-regulated significantly in zebrafish after treated with OLA. Besides, the anti-apoptotic and pro-apoptotic genes bcl-2/bax ratio was reduced. These results show that OLA exposure could cause severe developmental neurotoxicity in the early stages of zebrafish life and OLA might induce neurotoxicity by inhibiting the expression of neuro-developmental genes and promoting apoptosis.

To investigate the hemostasis effect of spleen-invigorating, Qi-replenishing and blood-arresting formula, on a zebrafish models with simvastatin-induced hemorrhage, and with symptom pattern caused by spleen failing to control blood, in terms of theory of Traditional Chinese Medicine (TCM).In the first experiment, 60 AB strain wild type zebrafishes were randomly assigned into two groups: normal group and model group. The model group was treated with 50 µM simvastatin for 24 h. The second experiment: The melanin allele mutated Albino strain zebrafishes were divided into normal, model, A group and B group. The observational parameters were as follows: blood flow, velocity of movement, hemorrhage ratio and improvement ratio of hemorrhage.Hemorrhage ratio: in the first experiment, brain hemorrhage ratio was 75%. In the second experiment, heart hemorrhage ratio was 65%. Blood flow: compared with the normal group, there was a significantly decrease in the model group (P0.001). Velocity of movement: in the first experimental, compared with the normal group, there was a significantly decrease in the model group (P0.001). Improvement ratio of hemorrhage: agents A had little effect in heart hemorrhage of the zebrafish; agents B could reduce heart hemorrhage ratio of the zebrafish, and increase the improvement ratio of hemorrhage.The manifestation of zebrafish model with simvastatin-induced hemorrhage is basically similar to that of the clinical symptom pattern caused by spleen's failure to control blood. The Spleen-invigorating, Qi-replenishing and Blood-arresting Formula can reduce the heart hemorrhage ratio of zebrafish induced by simvastatin, and increase the Improvement ratio of hemorrhage.

Tripterygium glycosides (TG) is isolated from an extensively used traditional Chinese medicine herb tripterygium roots and has been extensively used in the treatment of rheumatoid arthritis, nephrotic syndrome, hyperthyroidism and other diseases due to its anti-inflammatory and immunosuppressive effects. Hearing toxicity has been recently associated with TG use in human patients. In this study, authors assessed hearing toxicity and possible molecular toxic mechanisms of TG in a whole animal model. The maximum non-lethal concentration (MNLC) of TG on the zebrafish was 21 mg/L. TG induced zebrafish hair cell loss in a dose-dependent manner (p