Gam Le Thi Hong, Jensen Frank Bo, Huong Do Thi Thanh, Phuong Nguyen Thanh, Bayley Mark
College of Aquaculture and Fisheries, Can Tho University, Can Tho City, Viet Nam.
Department of Biology, University of Southern Denmark, Odense, Denmark.
Aquat Toxicol. 2018 Mar;196:124-131. doi: 10.1016/j.aquatox.2018.01.011. Epub 2018 Jan 31.
Nitrite and carbon dioxide are common environmental contaminants in the intensive aquaculture ponds used to farm clown knifefish (Chitala ornata) in the Mekong delta, Vietnam. Here we tested the hypothesis that hypercapnia reduces nitrite uptake across the gills, because pH regulation will reduce chloride uptake and hence nitrite uptake as the two ions compete for the same transport route via the branchial HCO/Cl exchanger. Fish fitted with arterial catheters were exposed to normocapnic/normoxic water (control), nitrite (1 mM), hypercapnia (21 mmHg CO), or combined hypercapnia (acclimated hypercapnia) and nitrite for 96 h. Blood was sampled to measure acid-base status, haemoglobin derivatives and plasma ions. Plasma nitrite increased for 48 h, but levels stayed below the exposure concentration, and subsequently decreased as a result of nitrite detoxification to nitrate. The total uptake of nitrite (evaluated as [NO] + [NO]) was significantly decreased in hypercapnia, in accordance with the hypothesis. Methemoglobin and nitrosylhemoglobin levels were similarly lower during hypercapnic compared to normocapnic nitrite exposure. The respiratory acidosis induced by hypercapnia was half-compensated by bicarbonate accumulation in 96 h, which was mainly chloride-mediated (i.e. reduced Cl influx via the branchial HCO/Cl exchanger). Plasma osmolality and main ions (Na, Cl) were significantly decreased by hypercapnia and by nitrite exposure, consistent with inhibition of active transport. We conclude that hypercapnia induces a long-lasting, and mainly chloride-mediated acid-base regulation that reduces the uptake of nitrite across the gills.
亚硝酸盐和二氧化碳是越南湄公河三角洲用于养殖刀鲇（Chitala ornata）的集约化养殖池塘中常见的环境污染物。在此，我们检验了如下假设：高碳酸血症会降低鳃对亚硝酸盐的摄取，因为pH调节会减少氯离子摄取，进而减少亚硝酸盐摄取，这是由于这两种离子通过鳃HCO/Cl交换器竞争相同的转运途径。给装有动脉导管的鱼暴露于常碳酸血症/常氧水（对照）、亚硝酸盐（1 mM）、高碳酸血症（21 mmHg CO）或高碳酸血症（适应的高碳酸血症）与亚硝酸盐联合环境中96小时。采集血液以测量酸碱状态、血红蛋白衍生物和血浆离子。血浆亚硝酸盐在48小时内升高，但水平保持在暴露浓度以下，随后由于亚硝酸盐解毒为硝酸盐而降低。根据假设，高碳酸血症中亚硝酸盐的总摄取量（以[NO] + [NO]评估）显著降低。与常碳酸血症亚硝酸盐暴露相比，高碳酸血症期间高铁血红蛋白和亚硝基血红蛋白水平同样较低。高碳酸血症诱导的呼吸性酸中毒在96小时内通过碳酸氢盐蓄积得到了部分代偿，这主要是由氯离子介导的（即通过鳃HCO/Cl交换器减少Cl内流）。高碳酸血症和亚硝酸盐暴露均显著降低了血浆渗透压和主要离子（Na、Cl），这与主动转运受到抑制一致。我们得出结论，高碳酸血症会诱导一种持久的、主要由氯离子介导的酸碱调节，从而减少鳃对亚硝酸盐的摄取。
