RESUMEN
An investigation of the influence of dietary copper (1, 5, 20 ppm) on toxicity of dietary lead (0 and 200 ppm) in the young male rat in a 4-week period indicated that as dietary copper increase so did the severity of lead toxicity. Evidence included increased lead concentration in kidney and a two- to threefold increase in the excretion of urinary delta-aminolevulinic acid. Liver copper concentration was also found to increase in rats receiving lead at the two lower copper levels. The data suggest that supplementary dietary copper doesnot lessen the severity of lead toxicity but rather exaggerates it.
Asunto(s)
Cobre/farmacología , Intoxicación por Plomo/metabolismo , Ácido Aminolevulínico/orina , Animales , Ceruloplasmina/metabolismo , Dieta , Riñón/metabolismo , Plomo/metabolismo , Hígado/metabolismo , Masculino , RatasRESUMEN
An investigation of the influence of dietary selenium (0.015, 0.05, 0.50, 1.0 ppm) on toxicity of dietary lead (0 and 200 ppm) in the young male rat indicated that selenium was mildly protective against the toxic effects of lead, but only up to 0.50 ppm selenium. At the excess selenium dietary level an exaggeration of lead toxicity was observed. Criteria employed to judge the effects of dietary selenium on lead toxicity included tissue lead concentration and urinary delta-aminolevulinic acid excretion. One exception to the exaggeration effect of excess selenium on lead toxicity was the protective effect of selenium on liver delta-aminolevulinic acid dehydratase activity. Since lead depressed kidney selenium concentration, lead may act as an antagonist to selenium metabolism.
Asunto(s)
Intoxicación por Plomo/prevención & control , Plomo/toxicidad , Selenio/farmacología , Animales , Huesos/metabolismo , Relación Dosis-Respuesta a Droga , Riñón/efectos de los fármacos , Riñón/metabolismo , Plomo/metabolismo , Hígado/efectos de los fármacos , Hígado/metabolismo , Masculino , Porfobilinógeno Sintasa/metabolismo , Ratas , Selenio/metabolismo , Selenio/uso terapéuticoRESUMEN
A series of five experiments was conducted with young male albino rats to investigate effects of various levels of dietary Ca, P and Mg on urinary cAMP excretion and kidney calcification. Urinary cAMP excretion was shown to be directly correlated with injected parathyroid (PT) hormone dose level and to be inversely associated with dietary Ca intake. Thus, cAMP excretion may be presumed to reflect PT activity in the young rat. Magnesium deficiency tended to reduce cAMP excretion, while P excess did not affect it. Each treatment induced kidney calcification. Calcium deficiency increased cAMP excretion irrespective of Mg status, although nephrocalcinosis appeared only in the Mg-deficient animals. These data support the view that nephrocalcinosis of dietary origin in the rat is not mediated by increased PT activity.