RESUMEN
Lead (Pb) is known to be highly poisonous, and the acute poisoning of Cd causes the abdominal pains, vomiting, and shock. The digestive and nervous symptom is observed in the chronic lead poisoning. It was also known that the defect in hemoglobin synthesis by Pb produce anemia. The release of Pb into the environment presents a source of exposure for wild animals. In this study, we examined the utility of a new Pb-monitoring index in mice administered Pb. A solution containing 0.02, 0.2, 2, or 4 ppm lead chloride (PbCl2) was administered intraperitoneally to mice, and the Pb contents of the kidney and liver were determined at designated time points. The mean Pb content of both organs increased depending on the administered Pb dosage. Although the results of control was near the detection limits, the administration of 4 ppm in 4 weeks resulted in Pb levels of 260 mg ppm/wet weight and 110 ppm wet weight in the kidney and liver, respectively. However, there were no significant relationships among administered dose, duration of Pb treatment, and liver or kidney Pb content. Then, values in all mice administered control or 0.02 mg Pb were located inside the ellipse, representing the confidence area of the new index, and values in all mice administered more than 2 mg Pb were located outside the ellipse. These results confirm that animals exposed to high concentrations of Pb would be detected by this new index.
Asunto(s)
Monitoreo del Ambiente , Contaminantes Ambientales/metabolismo , Riñón/metabolismo , Plomo/metabolismo , Hígado/metabolismo , Animales , Peso Corporal , Contaminación Ambiental , RatonesRESUMEN
Basic fibroblast growth factor (bFGF) has been thought to act as a neurotrophic factor during early developmental stages in various brain regions, including the hypothalamus. In the present paper, we have studied the effect of bFGF on peptide-containing neurons cultured from the postnatal (1-3 days and 14 days after birth) rat hypothalamus. The addition of bFGF, or acid FGF (aFGF), to serum-free culture medium increased both survival and neurite growth of growth hormone-releasing factor (GRF)-containing neurons. The potency of bFGF was more than 10 times as great as that of aFGF. Insulin-like growth factor I (IGF-I) did not have any significant effect on the survival of GRF neurons. Further, neither IGF-I nor aFGF modified the survival-promoting effect of bFGF on GRF neurons. bFGF promoted the survival of somatostatin- and vasoactive intestinal polypeptide-containing neurons, too.