Iftikar Fathima I, Matey Victoria, Wood Chris M
Department of Biology, McMaster University, Hamilton, Ontario L8S4K1, Canada.
Physiol Biochem Zool. 2010 Mar-Apr;83(2):343-55. doi: 10.1086/648566.
We utilized the rainbow trout, a hypoxia-intolerant freshwater teleost, to examine ionoregulatory changes at the gills during hypoxia. Progressive mild hypoxia led first to a significant elevation (by 21%) in J(Na)(influx) (measured with 22Na), but at 4-h hypoxia when PCO2 reached approximately 110 mmHg, there was a 79% depression in J(Na)(influx). Influx remained depressed during the first hour of normoxic recovery but was restored back to control rates thereafter; there were no significant changes in J(Na)(efflux) or J(Na)(net). A more prolonged (8 h) and severe hypoxic (approximately 80 mmHg) exposure induced a triphasic response whereby J(Na)(influx) was significantly elevated during the first hour, as during mild hypoxia, but returned to control rates during the subsequent 3 h. Thereafter, rates started to gradually increase and remained significantly elevated by about 38% through to 8 h of hypoxia. A similar triphasic trend was observed with J(Na)(efflux) but with larger changes than in J(Na)(influx), such that negative Na+ balance occurred during the hypoxic exposure. Net K+ loss rates to the water approximately doubled. There were no significant alterations in ammonia excretion rates in either of the hypoxia regimes. Branchial Na+/K+-ATPase activity did not change during 4 h at PO2 approximately 80 mmHg or return to normoxia; H+-ATPase activity also did not change during hypoxia but was significantly depressed by approximately 75% after 6 h of normoxic recovery. Scanning electron microscopy revealed that within 1 h of exposure to PO2 approximately 80 mmHg, exposed mitochondria-rich cell (MRC) numbers increased by 30%, while individual MRC exposed surface area and total MRC surface area both increased by three- to fourfold. MRC numbers had decreased below control levels by 4 h of hypoxia, but surface exposure remained elevated by approximately twofold, a response that persisted through 6 h of normoxic recovery. Environmental hypoxia induces complex changes in gill ionoregulatory function in this hypoxia-intolerant species that are very different from those recently reported in the hypoxia-tolerant Amazonian oscar.
我们利用虹鳟鱼（一种不耐受低氧的淡水硬骨鱼）来研究低氧期间鳃部的离子调节变化。逐渐加重的轻度低氧首先导致J(Na)(内流)显著升高（升高21%，用22Na测量），但在低氧4小时、PCO2达到约110 mmHg时，J(Na)(内流)降低了79%。在常氧恢复的第一个小时内，内流仍处于抑制状态，但此后恢复到对照速率；J(Na)(外流)或J(Na)(净流)没有显著变化。更长时间（8小时）和更严重的低氧（约80 mmHg）暴露诱导了一种三相反应，即J(Na)(内流)在第一个小时内显著升高，与轻度低氧时一样，但在随后的3小时内恢复到对照速率。此后，速率开始逐渐增加，并在低氧8小时时仍显著升高约38%。J(Na)(外流)也观察到类似的三相趋势，但变化比J(Na)(内流)更大，以至于在低氧暴露期间出现了负钠平衡。向水中的净钾流失率大约增加了一倍。在两种低氧状态下，氨排泄率均无显著变化。在PO2约80 mmHg下4小时或恢复到常氧期间，鳃部Na+/K+-ATP酶活性没有变化；H+-ATP酶活性在低氧期间也没有变化，但在常氧恢复6小时后显著降低约75%。扫描电子显微镜显示，暴露于PO2约80 mmHg 1小时内，富含线粒体的细胞（MRC）数量增加了30%，而单个MRC的暴露表面积和总MRC表面积均增加了三到四倍。低氧4小时时，MRC数量降至对照水平以下，但表面暴露仍升高约两倍，这种反应在常氧恢复6小时后持续存在。环境低氧在这种不耐受低氧的物种中诱导了鳃部离子调节功能的复杂变化，这与最近报道的耐低氧的亚马逊丽鱼科鱼非常不同。
