Abstract

Two- to 3.4-year-old, retired breeder, rabbits received repeated aluminum (Al) lactate or sodium (Na) lactate injections. All six rabbits receiving twenty 400 μmole Al/kg SC injections died, demonstrating much higher mortality than previously seen in younger rabbits. Subsequent rabbits receiving Al were dosed with 200 μmole/kg injections. Aluminum injections inhibited body weight gain. Renal function, as measured by creatinine clearance, in these rabbits was inferior to younger rabbits, perhaps contributing to the Al induced toxicity. Renal function decreased during Al injections suggesting a nephrotoxic effect of Al. Rabbits were tested for their ability to acquire, retain and extinguish a classically conditioned reflex, nictitating membrane extension. Rabbits which received Al acquired and retained the conditioned response less well than Na lactate injected rabbits. Impaired acquisition was evidenced by lower percent conditioned responses, more trials to 1 to 10 consecutive conditioned responses and longer conditioned response latencies. Aluminum injections produced significant elevations in tissue Al concentration in frontal gray and hippocampal brain as well as most peripheral tissues studied. Aluminum induced behavioral toxicity is greater in adult and aged rabbits than in young rabbits. Aged rabbits are more susceptible to Al induced mortality than adult or young rabbits.

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