Post Toxicity Screening of Dipropyl Phthalate on Early Vertebrate Development

Lim, Kang Young (2017) Post Toxicity Screening of Dipropyl Phthalate on Early Vertebrate Development. [Final Year Project Report] (Unpublished)

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Abstract

Dipropyl phthalate (DPrP) is one of the synthetic phthalate esters (PAEs) used as a plasticiser. Due to its weak bonding, it leaks out easily from the matrix of products, found in the consumer products and the environment. Certain family members of P AEs have been proved to be carcinogens and endocrine disrupt ors. Several studies showed that it could be estrogenic, antiestrogenic, or neither both. DPrP toxicity and toxicogenomic of vertebrate development are not well-known. The zebrafish was chosen as the animal model. The fertilised eggs were exposed to nine tested concentrations ofDPrP from 4-hour post fertilisation (hpf) to 96 hpf. The median lethal concentration (LC so) was 5.16 mg/L, between 5.03 mg/Land 5.30 mg/L with 95% confidence level. The lowest observed effect concentration (LOEC) was 4.86 mg/L while the no observed effect concentration (NOEC) was 4.65 mg/L. The adverse effects ofDPrP on morphology were uninflated swim bladder, pericardia! oedema, and yolk oedema. Other effects included craniofacial deformation, blood island, bent spine, shortened body, stretched heart, microphthalmia, and yolk opaque. The hatching rate of zebrafish was reduced with the increasing in the concentration ofDPrP. The results suggest that environment especially aquatic ecology could be affected by DPrP. Transthyretin gene (ttr) was the main study gene to discover DPrP impact on thyroid hormone. The expression level of ttr was examined at the transcriptional level. Total RNA was isolated from 96 hpf zebrafish embryos followed by semi-quantitative RT-PCR and agarose gel electrophoresis. Three concentrations of DPrP were tested for effect on ttr, which are 4.65 mg/L, 5.07 mg/L, and 5.70 mg/L. The transcriptional level of ttr reduced with the increasing of concentration of DPrP. Therefore, it is expected that DPrP could be endocrine disruptor through the downregulation of ttr.

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