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      Effects of pre-acclimation to aluminium on the physiology and swimming behaviour of juvenile rainbow trout (Oncorhynchus mykiss) during a pulsed exposure.

      Aquatic Toxicology (Amsterdam, Netherlands)
      Adaptation, Physiological, drug effects, Aluminum, blood, metabolism, toxicity, Animals, Behavior, Animal, Blood Cell Count, Blood Glucose, Chlorides, Fresh Water, Gills, Liver Glycogen, Oncorhynchus mykiss, physiology, Swimming

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          Abstract

          Anthropogenic acidification of the freshwater environment causes aluminium to be mobilised into the aquatic environment. When pH falls below 5.5, exposure to aluminium concentrations as low as 12.5 microg.l(-1) can cause serious physiological disturbances in freshwater fish. However, under constant laboratory exposures fish can acclimate and recover physiological status within 5-30 days. In reality, fish in the wild are likely to experience chronic sub-lethal exposure, with occasional elevations (pulses) to much higher levels. The experiment described here investigated the effects of an environmentally realistic, 4-day pulse exposure to a high level of aluminium (36 microg.l(-1)) in two groups of juvenile rainbow trout. One group was exposed to a lower level of aluminium (24 microg.l(-1)) for 16 days before and 10 days after the pulse ('aluminium-acclimated' fish). A second group was exposed to pH 5.2 alone for 16 days before and 10 days after the pulse ('aluminium-naïve' fish). A third group exposed to pH 5.2 alone for 30 days (no aluminium added) acted as controls. Triplicate groups of 24 juvenile rainbow trout (2.3-16.7 g) were randomly allocated to one of these three treatments. Swimming behaviour was monitored throughout and samples were taken on days 14, 20, 22, 26 and 30 for assessment of physiological status. No treatment effects were recorded in the control group (pH 5.2 alone). Fish in the 'aluminium-acclimated' treatment became hypo-active upon initiation of the exposure to 24 microg.l(-1) aluminium, but recovered after just 4 days of this exposure. Subsequent challenge on day 16 with the 36 microg.l(-1) aluminium 'pulse' caused these fish to became hypo-active again, but they recovered normal swimming behaviour whilst still subject to the 4-day pulse. The 'aluminium-naïve' fish also became hypo-active during the pulse exposure (36 microg.l(-1) aluminium). However, they did not exhibit any recovery of swimming behaviour, either during the pulse, or even 6 days after the cessation of the pulse, despite a rapid depuration of gill aluminium load (within 2 days of the pulse finishing). Mortality was low in the aluminium-acclimated fish (4%) and significantly higher in the aluminium-naïve fish (26%). Haematological disturbances were most extreme in the aluminium-naïve fish and had not recovered to control levels 6 days after the end of the pulse. This study provides new evidence, using behavioural responses, that previous exposure to low levels of aluminium may be an important factor abating the impact of aluminium on fish in the natural environment.

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