Tench exposed for 6 days to acid (pH5) hard water ([Ca2+] = 3.5 mmoll−1) in the presence of aluminium (2 mgl−1) showed a rapid decrease (within 3 h) in dorsal aortic Poo2 and a simultaneous rise in Pcoco2. Arterial oxygen content and haemoglobin-oxygen (Hb-O2) saturation decreased sharply, as did red cell [Hb], whereas blood haematocrit (Hct) and [Hb] increased. Red cell nucleoside triphosphate (NTP) content was reduced within 1 day through a selective reduction in guanosine triphosphate (GTP).

Although the rising Pcoco2 caused an extracellular acidosis (to which lactic acid production and perhaps H+ influx at the gills contributed), red cell pH increased compared to control values, mainly as a result of the decrease in Hb-O2 saturation. Plasma [Cl] declined, whereas [HCO3], [K+] and [Ca2+] increased. Ionic disturbances, however, were small compared to the changes in blood O2 transport, which appeared to correlate with high ambient [Ca2+].

Tench exhibited a high tolerance to the acid-Al exposure and most of the above parameters showed partial recovery within 1–2 days. In some specimens, however, the exposure was lethal because of an obstruction of gill function, and arterial blood became almost completely deoxygenated and showed very low pH values and high lactate concentrations, attesting to deep internal hypoxia.

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