Clifford Alexander M, Goss Greg G, Wilkie Michael P
Department of Biological Sciences, University of Alberta, Edmonton, Alberta, T6G 2E9, Canada; Bamfield Marine Sciences Centre, Bamfield, British Columbia, V0R 1B0, Canada.
Department of Biological Sciences, University of Alberta, Edmonton, Alberta, T6G 2E9, Canada; Bamfield Marine Sciences Centre, Bamfield, British Columbia, V0R 1B0, Canada.
Comp Biochem Physiol A Mol Integr Physiol. 2015 Apr;182:64-74. doi: 10.1016/j.cbpa.2014.12.010. Epub 2014 Dec 10.
The Pacific hagfish (Eptatretus stoutii) has an exceptional ability to both withstand and recover from exposure to high external ammonia (HEA). This tolerance is likely due to the feeding behavior of this scavenger, which feeds on intermittent food falls of carrion (e.g. fish, large marine mammals) during which time it may be exposed to high concentrations of total ammonia (T(Amm)=NH3+NH4(+)) while burrowed inside the decomposing carcass. Here we exposed hagfish to 20 mmol L(-1) T(Amm) for periods of up to 48 h and then let animals recover in ammonia-free seawater. During the 48 h HEA exposure period, plasma T(Amm) increased 100-fold to over 5000 μmol L(-1) while ammonia excretion (J(amm)) was transiently inhibited. This increase in plasma T(Amm) resulted from NH3 influx down massive inwardly directed ΔP(NH3) gradients, which also led to a short-lived metabolic alkalosis. Plasma [T(Amm)] stabilized after 24-48 h, possibly through a reduction in NH3 permeability across the body surface, which lowered NH3 influx. Ammonia balance was subsequently maintained through the re-establishment of J(amm) against an inwardly directed ΔP(NH3). Calculations of the Nernst potential for ammonia strongly indicated that J(amm) was also taking place against a large inwardly directed NH4(+) electrochemical gradient. Recovery from HEA in ammonia-free water was characterized by a large ammonia washout, and the restoration of plasma TAmm concentrations to near control concentrations. Ammonia clearance was also accompanied by a residual metabolic acidosis, which likely offset the ammonia-induced metabolic alkalosis seen in the early stages of HEA exposure. We conclude that restoration of J(amm) by the Pacific hagfish during ammonia exposure likely involves secondary active transport of NH4(+), possibly mediated by Na(+)/NH4(+) (H(+)) exchange.
太平洋盲鳗(Eptatretus stoutii)具有非凡的能力,既能承受高浓度外部氨(HEA)暴露,又能从这种暴露中恢复。这种耐受性可能归因于这种食腐动物的摄食行为,它以腐肉(如鱼类、大型海洋哺乳动物)的间歇性食物掉落为食,在此期间,当它钻入正在分解的尸体内部时,可能会接触到高浓度的总氨(T(Amm)=NH₃ + NH₄⁺)。在这里,我们将盲鳗暴露于20 mmol L⁻¹的T(Amm)中长达48小时,然后让动物在无氨海水中恢复。在48小时的HEA暴露期间,血浆T(Amm)增加了100倍,超过5000 μmol L⁻¹,而氨排泄(J(amm))被短暂抑制。血浆T(Amm)的这种增加是由于NH₃顺着巨大的内向ΔP(NH₃)梯度流入,这也导致了短暂的代谢性碱中毒。24 - 48小时后血浆[T(Amm)]稳定下来,可能是通过降低体表NH₃的通透性,从而减少了NH₃的流入。随后通过重新建立对抗内向ΔP(NH₃)的J(amm)来维持氨平衡。氨能斯特电位的计算强烈表明,J(amm)也是逆着一个大的内向NH₄⁺电化学梯度进行的。在无氨水中从HEA恢复的特征是大量的氨排出,以及血浆TAmm浓度恢复到接近对照浓度。氨清除还伴随着残余的代谢性酸中毒,这可能抵消了HEA暴露早期出现的氨诱导的代谢性碱中毒。我们得出结论,太平洋盲鳗在氨暴露期间恢复J(amm)可能涉及NH₄⁺的继发性主动转运,可能由Na⁺/NH₄⁺(H⁺)交换介导。