The gills are osmorespiratory organs of aquatic organisms and the prime target of environmentally induced hypoxia. We have studied the impact of severe hypoxia (0.5 mg O2/L) on the ionic transport across posterior gills of Carcinus maenas acclimated to 12 ppt seawater (DSW). The short-circuit current (Isc) across hemilamellae from gills i.e. active ion transport was studied in micro Ussing chambers. Hypoxia induced by deoxygenation of the basolateral side, and not the apical side, resulted in time-dependent inhibition of Isc and full recovery of Isc after reoxygenation. Exposure of the crabs to severe 7 h hypoxia decreased the specific activity of Na+,K+-ATPase in the gills by 36%. Full recovery of enzyme activity occurred in fasted crabs after 3 days of reoxygenation. The intensity of Western blotting bands was not different in the gills of oxygenated, hypoxic and reoxygenated crabs. The reversible, nonspecific blocker of K+ channels Cs and hypoxia inhibited over 90% of Isc which is after reoxygenation fully recovered. The specific blocker of Cl− channels NPPB [5-nitro-2-(3-phenylpropylamino)benzoic acid] blocked Isc by 68.5%. Only the rest of not inhibited Isc in aerated saline was blocked by hypoxia and recovered after reoxygenation. The activity of the antioxidant enzyme catalase was not changed during hypoxia and reoxygenation kept the high enzyme activity in the gills at the level of crabs acclimated to DSW. As a response to hypoxia the presence of 2 mM H2O2 induce an initial slight transient decrease of Isc followed by a rise and after reoxygenation fully recovered Isc. Incubation of hemilamellae with the antioxidant derivative Trolox did not affect the inhibition of Isc by hypoxia.

中文翻译：

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缺氧减弱了 Carcinus maenas 分离的鳃上皮中的离子转运

鳃是水生生物的渗透呼吸器官，也是环境诱导缺氧的主要目标。我们研究了严重缺氧 (0.5 mg O2/L) 对通过适应 12 ppt 海水 (DSW) 的 Carcinus maenas 后鳃的离子传输的影响。在微型 Ussing 室中研究了来自鳃的半薄片上的短路电流 (Isc)，即活性离子传输。由基底外侧而非顶端脱氧引起的缺氧导致 Isc 的时间依赖性抑制和再氧合后 Isc 的完全恢复。螃蟹暴露于严重缺氧 7 小时后，鳃中 Na+,K+-ATPase 的比活性降低了 36%。再充氧 3 天后，禁食螃蟹的酶活性完全恢复。含氧、缺氧和复氧螃蟹鳃中蛋白质印迹条带的强度没有差异。K+ 通道 Cs 和缺氧的可逆、非特异性阻断剂抑制了 90% 以上的 Isc，这是在再充氧后完全恢复的。Cl- 通道的特异性阻断剂 NPPB [5-nitro-2-(3-phenylpropylamino)benzoic acid] 将 Isc 阻断了 68.5%。只有其余未受抑制的充气盐水中的 Isc 被缺氧阻断并在复氧后恢复。抗氧化酶过氧化氢酶的活性在缺氧期间没有改变，复氧使鳃中的高酶活性保持在适应 DSW 的螃蟹水平。作为对缺氧的反应，2 mM H2O2 的存在诱导 Isc 的初始轻微短暂下降，然后升高，再充氧后完全恢复 Isc。