Ammonia affects brain nitrogen metabolism but not hydration status in the Gulf toadfish (Opsanus beta).
Ammonia affects brain nitrogen metabolism but not hydration status in the Gulf toadfish (Opsanus beta).
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氨会影响海湾蟾蜍（Opsanus beta）的大脑氮代谢，但不会影响水合状态。
DOI：
10.1016/j.aquatox.2005.05.003
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发表时间：
2005
期刊：
影响因子：
--
通讯作者：
Walsh,PatrickJ
中科院分区：
文献类型：
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作者：
Veauvy,ClemenceM;McDonald,MDanielle;VanAudekerke,Johan;Vanhoutte,Greet;VanCamp,Nadja;VanderLinden,Annemie;Walsh,PatrickJ
实验室啮齿类动物通过将氨注入血液而造成高氨血症，表现出脑细胞肿胀和颅内压升高的症状。这些症状可能部分由脑谷氨酰胺合成酶（GS）自然地将氨解毒为谷氨酰胺时形成的脑谷氨酰胺增加引起。先前对海湾蟾鱼（Opsanus beta）的研究表明，尽管脑谷氨酰胺增加，但它对高氨暴露（HAE）具有抗性（96 h LC50= 10 mM）。本研究试图解决O.β是由面对谷氨酰胺浓度变化时脑水的特殊处理介导的。用GS抑制剂甲硫氨酸亚砜亚胺（MSO）调节谷氨酰胺浓度，用磁共振成像（MRI）评估脑水状态。氨或MSO治疗对血液酸碱参数无显著影响。暴露于3.5mM氯化铵海水中16或40小时导致脑氨（3倍）和谷氨酰胺（2倍）平行增加，脑谷氨酸（1.3倍）减少。用MSO预处理防止氨诱导的谷氨酰胺和谷氨酸浓度的变化。HAE还诱导血浆渗透压升高（7%），这可能是由于代谢调节过程的干扰，但未导致更广泛的全身脱水，如肌肉水分分析所示。脑谷氨酰胺的增加与蟾鱼暴露于3.5mM氨长达40小时或甚至在10，20和30mM氨连续和在每个浓度下1小时的脑水的任何变化无关。缺乏脑水积累意味着蟾鱼的氨毒性似乎是通过脑肿胀以外的途径。此外，用MSO预处理的蟾鱼不能在正常的亚致死暴露于3.5mM氨40小时后存活。MSO对氨毒性的增强表明GS功能对该物种的氨耐受性至关重要。
Laboratory rodents made hyperammonemic by infusing ammonia into the blood show symptoms of brain cell swelling and increased intracranial pressure. These symptoms could be caused in part by an increase in brain glutamine formed when brain glutamine synthetase (GS) naturally detoxifies ammonia to glutamine. Previous studies on the Gulf toadfish (Opsanus beta) demonstrated that it is resistant to high ammonia exposure (HAE) (96h LC50=10mM) despite an increase in brain glutamine. This study attempts to resolve whether the resistance of O. beta is mediated by special handling of brain water in the face of changing glutamine concentrations. Methionine sulfoximine (MSO), an inhibitor of GS, was used to pharmacologically manipulate glutamine concentrations, and magnetic resonance imaging (MRI) was used to assess the status of brain water. Ammonia or MSO treatment did not substantially affect blood acid–base parameters. Exposure to 3.5mM ammonium chloride in seawater for 16 or 40h resulted in a parallel increase in brain ammonia (3-fold) and glutamine (2-fold) and a decrease in brain glutamate (1.3-fold). Pre-treatment with MSO prevented ammonia-induced changes in glutamine and glutamate concentrations. HAE also induced an increase in plasma osmolality (by 7%) which was probably due to a disturbance of osmoregulatory processes but which did not result in broader whole body dehydration as indicated by muscle water analysis. The increase in brain glutamine was not associated with any changes in brain water in toadfish exposed to 3.5mM ammonia for up to 40h or even at 10, 20 and 30mM ammonia consecutively and for one hour in each concentration. The lack of brain water accumulation implies that ammonia toxicity in toadfish appears to be via pathways other than cerebral swelling. Furthermore, toadfish pre-treated with MSO did not survive a normally sub-lethal exposure to 3.5mM ammonia for 40h. The enhancement of ammonia toxicity by MSO suggests that GS function is critical to ammonia tolerance in this species.