Fish tissue from Labeo capensis and sediment core samples from three dams in the Mooi River catchment area were collected and analysed for Cd and Pb by electro-thermal AAS, and for Cu and Zn by flame AAS. The highest Cd concentrations were found in the clay fractions in all three dams, with a range between 66.0 µg·g -1 and 107 µg·g -1 . Lead concentrations below 34 µg·g -1 were found in all six sediment types from Klerkskraal Dam, while Potchefstroom Dam had the highest lead levels (range: 34 -62 µg·g -1 ) for the six sediment fractions and also for all the fish tissue types (range: 38 -79 µg·g -1 ). Lead alkyls from motorboat exhausts were probably responsible for the high lead concentrations in the sediment of Potchefstroom Dam and in the mudfish tissues. The mean zinc concentrations from five of the six fractions in Boskop Dam were significantly higher compared to the other dams, with a range between 25 µg·g -1 to 59 µg·g -1 . The combined six fractions were between five and 100 times lower in concentration when compared to the pelitic sediment samples from sediments at the Lebanon and West Driefontein mines in the Mooi River catchment. Copper concentrations in dam sediment from the six fractions for the three dams, ranging between 11µg·g -1 to 36 µg·g -1 , were higher when compared with copper levels worldwide. The kidneys, gills and liver had the highest levels of Cd, Pb and Cu respectively compared to other tissues from L. capensis, while the gills had the highest concentration of Zn. In conclusion, higher than normal metal concentrations were found in Boskop Dam sediments, which could be linked to gold mine operations inside the Mooi River catchment area. Lead, Cd, Cu and Zn concentrations in L. capensis tissues were much lower compared to reported data on South African fish, but on par with world levels. The percentage of uranium present in sediment samples (analysed by energy dispersive X-ray spectrometry) from the three dams was 9.0 % (SD 2.1%). In sediment it was found that cation exchange capacity measurements and the dolomitic hard water and high pH of the Mooi River water effectively 'detoxified' Cd and Pb, forming insoluble complexation products buried in the sediment.

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 CaCO 3 ), cadmium (Cd) applied as CdCl 2 , precipitates completely out but in very soft water (16.5 mg·l -1 as Ca CO 3 ), 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 (ΜO 2 ) by more than 30% compared to resting oxygen consumption levels. In hard water no change in the ΜO 2 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 ΜO 2 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 µg Cd·g -1 accumulates per gram dried gill mass when fish are exposed to 20 mg Cd·l -1 in hard water. For soft water the Cd accumulation is about twice as much. In liver tissue more than 60 µg 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·l -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 ΜO 2 returns to normal resting levels 6 h after handling stress. It is concluded from the results that ΜO 2 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.

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