This study aims to evaluate the impact of adding different items in individually ventilated rat cages on the animal's activity, cardiovascular parameters and faecal stress indicators. The following three cage items made of aspen were compared: a cross made of two intersecting boards, a similar cross where drilled holes were loaded with food pellets (restricted feeding) and a rectangular tube. Male rats of the strains BN and F344 (n ¼ 12) were housed in groups of three; one rat in each group was implanted with a telemetric transponder to measure mean arterial pressure (MAP) and heart rate (HR). In a crossover design, each group spent 14 days with each type of cage furniture, thereafter faecal pellets were collected for faecal analyses. The means of activity and means and coefficient of variation for MAP and HR were calculated for days 2, 6, 10 and 14. As a way of determining which of the statistically significant MAP and HR mean changes were biologically meaningful, the night -day differences of the controls on day 14 were used. Both board types lowered MAP of F344 rats; hence dividing walls seem beneficial for F344 welfare. None of the MAP or HR differences in BN rats were biologically significant. No statistically significant differences in faecal corticosterone or IgA excretion were detected. In conclusion, provision of general recommendations with respect to cage furniture for rat cages is complicated because there is a clear genetic component involved in how animals respond to these structures.
The effects of aluminium lactate (Al-lactate) on the rat cerebral synaptosome integral proteins adenosinetriphosphatase (ATPase) and acetylcholinesterase(AChE) were studied in vitro and in vivo. Coexposure with ethanol (EtOH) was studied in both situations. Isolation of synaptosomes was carried out using isoosmotic Percoll gradients. In in vitro experiments, the synaptosomes were exposed to different concentrations of Al-lactate in the incubation mixture. Al-lactate caused decreases in total ATPase and AChE activities concentration dependently. The decrease in ATP activity started at 0.2 mM concentration, and concentration for the 50% decrease of the enzyme activity (EC50 ) was 1.1 mM. The decrease in AChE activity started at 5-10 mM concentration, and the EC50 value was 15.8 mM. Coexposure with ethanol (2 mM) increased the EC50 values similarly in both cases. After 90-day oral exposure of rats to Al-lactate (91.8 mg/kg/day), the serum aluminium level was 0.9-1.3 ptM/l. Coexposure with EtOH(3.0 g/kg/day) did not significantly increase the blood Al(0.7 2.2 pM/l). Aluminium exposure caused a decrease in the blood EtOH concentration (0.6 mM/1) compared with blood EtOH (12.3 mM/1) in the rats exposed to ethanol only. In the rats studied 2 weeks after the Al exposure, the activities of ATPase and AChE were significantly lower than in the rats studied immediately after the exposure. Correspondingly, a significant decrease in AChE activity was found in Al and EtOH-exposed rats, but in the control rats there were no differences between the study groups. Immediately after the 90-day dosing, the exposed rats did not differ significantly from the control rats. Based on the in vitro results, the neural membrane integral proteins ATPase and AChE may be considered as targets for the effects of aluminium and ethanol. Ninety-day in vivo exposure of rats to aluminium caused decrease in ATPase and AChE activities, detectable 2 weeks after the exposure.
In this in vitro study, changes in the activity of the neural membrane integral protein, ATPase, were recorded after the exposure of isolated synaptosomes to different concentrations of aluminium and lead. Both total ATPase activity and Mg2+-ATPase activity were studied. A specific mouse strain, heterozygous for a glial cell line-derived neurotrophic factor (GDNF), and the corresponding wild-type mouse cerebral tissue, were used for the synaptosome isolations. The ATPase activities of the GDNF+/– mouse synaptosomes were compared with those of wild-type synaptosomes. The decrease in total ATPase activity was similar in both types of synaptosomes, but after exposure to aluminium, the decrease of Mg2+-ATPase activity in the GDNF+/– synaptosomes was smaller than that in the wild-type synaptosomes. After exposure to lead, the protective effect of GDNF was not so clear. The synaptosomal effects of lead were already found at concentrations lower than those where cell toxicity appeared in SHSY5Y cell cultures. Thus, synaptosomal ATPase activity was considered to be a sensitive marker for the detection of lead-induced neurotoxicity.
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