汞(Hg)是一种危险和持久的微量元素。它的有机和剧毒形式,甲基汞(MeHg),很容易穿过生物膜并在生物群中积累。然而,了解鱼类饮食中甲基汞中毒的机制仍然是一个挑战。对幼年的白海底进行了时程实验,Diplodussargus(Linnaeus,1758),暴露于饲料中实际水平的甲基汞含量(8.7μgg-1,干重),包括暴露期(E;7天和14天)和暴露后(PE;28天)。在E期间,ill和肝脏中的总Hg水平随着时间的推移而增加,而在PE中则显着降低(尽管仅在ill中达到了对照鱼的水平),肝脏表现出比g更高的水平(2.7倍)。基于核磁共振(NMR)的代谢组学揭示了鱼类器官之间的多种且通常不同的代谢变化。ill表现出蛋白质分解代谢,胆碱能神经传递障碍,以及渗透调节和脂质和能量代谢的变化。然而,饮食中的甲基汞暴露会引起肝脏中蛋白质代谢的改变,氨基酸减少,可能会激活防御策略。PE允许两个器官的部分恢复,即使发生氧化应激和能量代谢的变化。总的来说,这些发现根据其对汞暴露的敏感性支持器官特异性反应,指出在生物监测研究中获得的适应症也可能取决于所选择的器官。
Mercury (Hg) is a dangerous and persistent trace element. Its organic and highly toxic form, methylmercury (MeHg), easily crosses biological membranes and accumulates in biota. Nevertheless, understanding the mechanisms of dietary MeHg toxicity in fish remains a challenge. A time-course experiment was conducted with juvenile white seabreams, Diplodus sargus (Linnaeus, 1758), exposed to realistic levels of MeHg in feed (8.7 μg g-1, dry weight), comprising exposure (E; 7 and 14 days) and post-exposure (PE; 28 days) periods. Total Hg levels increased with time in gills and liver during E and decreased significantly in PE (though levels of control fish were reached only for gills), with liver exhibiting higher levels (2.7 times) than gills. Nuclear magnetic resonance (NMR)-based metabolomics revealed multiple and often differential metabolic changes between fish organs. Gills exhibited protein catabolism, disturbances in cholinergic neurotransmission, and changes in osmoregulation and lipid and energy metabolism. However, dietary MeHg exposure provoked altered protein metabolism in the liver with decreased amino acids, likely for activation of defensive strategies. PE allowed for the partial recovery of both organs, even if with occurrence of oxidative stress and changes of energy metabolism. Overall, these findings support organ-specific responses according to their sensitivity to Hg exposure, pointing out that indications obtained in biomonitoring studies may depend also on the selected organ.