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Low-dose lead encephalopathy in the suckling rat

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Summary

Retardation of growth has often confounded the interpretation of the results from experimental studies on lead intoxication. An attempt was therefore made to establish a daily dose of lead which, when given to suckling rags, results in a lead encephalopathy without concomitant reduction in body weight. Lead was administered i.p. as lead nitrate. Experimental animals were given 25, 10, or 5 mg lead nitrate/kg b.wt. daily during the first 20 days postnatally (p.n.). One group was given 10 mg/kg daily during the first 15 days. Controls were injected with vehicle without lead nitrate. Mortality was high in the group given 25 mg/kg b.wt. daily. Animals in this group exhibited a marked weight loss after 10 days. A slight but significant reduction in body weight was seen at 20 days in animals receiving 10 mg/kg b.wt. from day 1 to 20. The body weight gain of animals given 10 mg/kg during 15 days and of animals given 5 mg/kg during 20 days did not significantly differ from that of controls. Lead content in blood and brain was determined using a Carbon Rod Atomizer. Lead levels were elevated in all experimental animals. Light-microscopic findings in the cerebellum of animals given 25 and 10 mg/kg b.wt. daily were similar to those previously reported in experimental lead encephalopathy. The changes were dose-dependent, lesions being devastating in rats given 25 mg/kg b.wt. daily and discrete in rats given 10 mg/kg b.wt. daily. No pathologic change could be demonstrated on the light-microscopic level in the cerebellum or cerebrum of rats given 5 mg/kg b.wt. daily. The lack of growth retardation in encephalopathic rats makes the model valuable for further investigations on lead neurotoxicity.

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Supported by grants from the Swedish Medical Research Council, project nos. 03488 (to P. Sourander) and 6345 (to N. G. Conradi) and from the Medical Faculty, University of Göteborg, Sweden

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Sundström, R., Conradi, N.G. & Sourander, P. Low-dose lead encephalopathy in the suckling rat. Acta Neuropathol 60, 1–8 (1983). https://doi.org/10.1007/BF00685340

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