Water hardness and the effects of Cd on oxygen consumption, plasma chlorides and bioaccumulation in <i>Tilapia sparrmanii</i>

Abstract

Closed system respirometry was performed on captive juvenile (30 + 8 g; mean + S.E.M) Tilapia sparrmanii exposed for 96 h to low (1 mg.l^-1) and high (20 mg.l^-1) levels of cadmium in soft and hard water. In hard water (235 mg.l^-1 as CaCO₃), cadmium (Cd) applied as CdCl₂, precipitates completely out but in very soft water (16.5 mg.l^-1 as Ca-CO₃ ), 23% of Cd is in solution 96 h after it was dissolved. Cadmium complexation is not caused by the presence of chlorides but probably depends on carbonates and sulphates present in Mooi River water. Handling stress, that lasts for at least 6 h, increased the specific oxygen consumption rate of T. sparrmanii (MO₂) by more than 30% compared to resting oxygen consumption levels. In hard water no change in the MO₂ was found when T. sparrmanii was exposed to 1, 5, 10, or 20 mg of Cd.l^-1 of water. In soft alkaline water all fish died when exposed for 96 h in 20 mg Cd.l^-1 . For 10 mg Cd.l^-1, the MO₂ was reduced significantly (p< 0.05) by 30%. The percentage cadmium dissolved in hard water was, after 96 h, below 1%, 96 h after it had been dissolved. About 2 000 g Cd.g^-1 accumulates per gram dried gill mass when fish are exposed to 20 mg Cd.g^-1 in hard water. For soft water the Cd accumulation is about twice as much. In liver tissue more than 60 g Cd accumulates per gram dried liver mass in hard water. In soft water the accumulation was three times as much. Blood plasma chlorides decreased from a mean of 130 mmol to 60 mmol when exposed to 20 mg Cd.g^-1 in soft water. The differences were statistically significant (P< 0.05). No decrease in blood plasma chlorides was found in hard water when fish were exposed to 20 mg Cd. l^-1 of water. Fish handling reduces the oxygen consumption rate by 35% but MO₂ returns to normal resting levels 6 h after handling stress. It is concluded from the results that MO₂ and blood chlorides can be used as parameters for Cd toxicity in a 96 h exposure period provided that the precipitation of Cd in the water is known and the pH of the water is monitored.


Water SA Vol.30(1): 57-64