碩士 / 國立臺灣大學 / 農業化學研究所 / 100 / Propiconazole is an environmentally important fungicide widely used in agriculture to prevent fungal growth on grasses, fruits, vegetables, cereals or seeds. It is frequently detected in wastewater, rivers and surface water at the μg/L level. Studies have demonstrated propiconazole is hepatotoxic and hepatotumorigenic in mice and induces oxidative stress (OS) in aquatic animals. The objective of this study is to understand modes of propiconazole-induced OS associated with hepatocarcinogenesis using early life stages of Japanese medaka (Oryzias latipes) and p53 mutant as model organisms. We have treated larvae of wildtype or p53 mutant medaka (14 day post hatching, dph) with propiconazole solutions at sub-lethal concentrations (2.5, 25 and 250 μg/L) for a 28-day continuous aqueous exposure and then reared fish in embryo rearing medium until adults. At each time point, wildtype larvae were harvested for analyses of intracellular reactive oxygen species (ROS) levels and biomarker assays of OS and oxidative damages. Both strains of matured fish were sacrificed for histopathology analyses. Our results show that propiconazole induced intracellular ROS levels during 14-35 day’s exposure especially at higher concentration in wildtype larvae. A dose-dependent increase in glutathione transferase (GST) activity was revealed, while catalase (CAT) and superoxide dismutase (SOD) activities were inhibited with the dosage during the exposure period. Also, CAT and SOD activities were recovered to the control level without the propiconazole exposure. Also propiconazole were induced malondialdehyde and protein carbonyl groups contents in 28 and 14 day’s exposure respectively at 250 μg/L treatment. These results indicate that propiconazole can induce ROS and cause OS in fish, and result in oxidative injury. However, the propiconazole induced-OS or injury could be recovered if stressor was removed, but some oxidative damage may be irreversible and may result in carcinogenesis in fish. The adults of wildtype medaka fish didn’t have significant pathological changes in liver, but propiconazole induced hepatocellular vaculoation, spongiosis hepatis, hepatic cyst and eosinophilic foci in livers of p53 adults. We also found livers of p53 mutant had macrophage accumulation that may lead to chornic inflammation. Overall, propiconazole induced oxidative stress and oxidative injury and these promoted hepatocarcinogenesis in medaka fish.
| Identifer | oai:union.ndltd.org:TW/100NTU05406011 |
| Date | January 2012 |
| Creators | Tzu-Yi Tu, 塗子毅 |
| Contributors | 陳佩貞 |
| Source Sets | National Digital Library of Theses and Dissertations in Taiwan |
| Language | zh-TW |
| Detected Language | English |
| Type | 學位論文 ; thesis |
| Format | 88 |
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