Interactive Effects of 17α-ethinylestradiol (EE2) and Hypoxia on Impairment of Testicular Functions in Male Marine Medaka Fish
DescriptionTo date, over 600 hypoxic zones (< 2 mg O2 L-1) spanning hundreds of thousands of square kilometers are reported worldwide. The number has increased significantly in recent decades, and a major increase in the number of hypoxic areas in Asia is predicted for the coming decade. Aquatic hypoxia has caused mass mortality of marine animals, declines in fisheries production, and major changes in species composition, and community structure over large areas. Declines in fish populations and the elimination of sensitive fish species is likely caused by decreases in reproductive success and fitness resulting from hypoxia, and with rapid coastal development, hypoxia is likely to worsen in the future, thereby threatening the sustainability of natural populations. Recent laboratory studies by our group and field studies by others have shown that hypoxia is a potent agent of endocrine disruption and can severely impair sexual differentiation and reproductive functions in fish. Endocrine disrupting chemicals (EDCs) comprise a diverse group of synthetic or natural compounds that are widespread in the aquatic environment and are known to adversely affect sexual development and reproductive functions in fishes. Much research has focused on the adverse impact of 17α-ethinylestradiol (EE2), a potent synthetic estrogen, because of its growing usage in human medicine and livestock farming activities, which has caused widespread damage in the aquatic environment. Despite the fact that hypoxia and EE2 stresses are widespread problems in aquatic environments worldwide, the combined effects of these two stressors on aquatic animals and ecosystem health are still poorly understood. Based on the recent successes of our group in developing the marine medaka (Oryzias melastigma) as a marine model organism (along with the corresponding genetic tools and resources) for ecotoxicogenomics, we propose to utilize the marine medaka fish model to extend our understanding of the combined effects of EE2 (a model estrogenic EDC) and hypoxia on testicular and reproductive functions in male medaka fish. It is hypothesized that the adverse effect of environmentally relevant concentrations of EE2 on reproductive functions in male fish will be exacerbated in the presence of hypoxic stress, and is underpinned by the activation of specific toxicity pathways. It is envisaged that the use of an ecotoxicogenomic approach to investigate the modes of testicular toxicity in the marine medaka will uncover some novel biomarkers that are of relevance for the development of risk assessment methodologies.
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