Mechanisms of nitrogen handling, toxicity and tolerance in fishes

我研究的总体目标是确定鱼类如何产生和排泄代谢废物，如氨和尿素，以及它们如何应对这些产品的潜在毒性积累。剧毒的氨是由蛋白质分解产生的，必须排出或转化为毒性较低的产物，如尿素。鱼类在进食后会积累氨，但当通过鳃的排泄被改变的水化学（例如b> pH值）或由自然（例如有机物质分解）或人为来源（例如污水和工业废水，农业径流）引起的水氨升高而受阻时，氨也会积累。在哺乳动物中，氨升高是由肝脏疾病引起的，并可能导致脑损伤或死亡。虽然氨靶向中枢神经系统（CNS），但其毒性机制尚不清楚。我的长期目标是确定氨和其他代谢废物的积累如何对鱼类的生理过程产生不利影响。我的大部分工作将集中在海七鳃鳗身上，它们生命的前半部分是滤食性幼虫，然后蜕变为以鱼类血液为食的寄生虫。我之前的研究表明，当寄生七鳃鳗以鲨鱼和鳟鱼的血液为食时，摄食会极大地刺激它们体内氨和尿素的排泄。在此基础上，我未来5年的目标是：

The overall goal of my research is to determine how fishes produce and excrete metabolic wastes such as ammonia and urea, and how they cope with potentially toxic build-ups of these products. Highly toxic ammonia arises from the breakdown of protein, and must be excreted or converted to less toxic products such as urea. Ammonia accumulates in fishes following feeding, but also when excretion via the gill is blocked by altered water chemistry (e.g. > pH) or elevated water ammonia arising from natural (e.g. decomposition of organic material) or anthropogenic sources (e.g. sewage and industrial effluent, agricultural run-off). In mammals, elevated ammonia results from liver disease, and can cause brain damage or death. Although ammonia targets the central nervous system (CNS), its mechanism of toxicity is unresolved. My long-term goal is to determine how build-ups of ammonia and other metabolic wastes adversely affect physiological processes in fishes. Much of my work will focus upon sea lampreys, who spend the first part of their life as filter-feeding larvae before metamorphosing into parasites that feed on the blood of fishes. My previous research demonstrated that feeding profoundly stimulated ammonia and urea excretion in parasitic lampreys as they fed on the blood of sharks and trout. Building upon this work, my OBJECTIVES for the next 5 years are to: