Lead acetate

About: Lead acetate is a research topic. Over the lifetime, 2636 publications have been published within this topic receiving 69739 citations.

Effect of inorganic lead exposure on myelination in the rat

Abstract: The effect of defined lead burdens on myelination of the central and peripheral nervous systems was studied in neonatal Long-Evans rats. Pups were exposed to inorganic lead (100 or 400 mg Pb as lead acetate/kg body wt/day by gastric intubation) from day 2 following birth to 30 days of age. Accumulation of myelin in forebrain was not affected by the 100-mg dosage, but at the 400 mg/kg dosage level, myelin accumulation was reduced by approximately 42% on a per gram forebrain basis relative to vehicle-intubated animals. The deficit was over 50% on a per forebrain basis, since there was also a slight reduction in brain weight. This lead effect was observed at both 15 and 30 days of age. Accumulation of myelin in optic nerve (determined on the basis of proteolipid protein concentration) was also reduced by 30% relative to controls by this dosage level. However, myelination in sciatic nerve (determined on the basis of P0 protein concentration) was not affected by this exposure regimen. Myelin deficits were greater than could be accounted for by undernutrition arising secondary to lead exposure and were not due to a developmental delay in the onset of myelination.

Alleviative effect of selenium on inflammatory damage caused by lead via inhibiting inflammatory factors and heat shock proteins in chicken testes.

Abstract: The aim of this study was to investigate ameliorative effect of selenium (Se) on lead (Pb)-induced inflammatory damage in chicken testes. One hundred eighty 7-day-old male chickens were randomly assigned into the control group, the Se group, the Pb group, and the Pb/Se group. Lead acetate was added in drinking water (350 mg/L Pb). Sodium selenite was added in the standard commercial diet (1 mg/kg Se). On the 30th, 60th, and 90th days of the experiment, 15 chickens of each group were euthanized. Inductively coupled plasma mass spectrometry, hematoxylin and eosin staining, real-time quantitative PCR, and Western blot were used. The results indicated that excess Pb increased nitric oxide content; inducible nitric oxide synthase (iNOS) activity; nuclear factor-kappa B (NF-κB), tumor necrosis factor-α, cyclooxygenase-2, prostaglandin E synthases, and iNOS mRNA levels in a time-dependent manner; NF-κB, iNOS, heat shock protein (HSP) 60, HSP70, and HSP90 protein levels; and Pb concentration. Excess Pb decreased Se concentration and induced histological changes. Se-alleviated Pb caused all of the above changes. Se improved Pb-caused inflammatory damage by decreasing the expression of inflammatory factors and heat shock proteins in the chicken testes. Our results provided theoretical basis of an alleviative effect of Se on Pb-induced bird testis damage.

Maternal lead exposure produces long-term enhancement of dopaminergic reactivity in rat offspring.

Abstract: To determine the effect of prenatal lead exposure on brain monoaminergic systems, pregnant rats were given tap water containing 250 ppm lead acetate, for the duration of pregnancy, while tap water without lead (Pb(2+)) was substituted at birth. Control rats were derived from dams that consumed tap water during pregnancy, and had no exposure to lead afterwards. At 12 weeks after birth, Pb(2+) content of brain cortex was increased 3- to 4-fold (P < 0.05). At this time the endogenous striatal levels of 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid were 19% lower in Pb(2+) exposed rats (P < 0.05), while there was no change in the striatal level of dopamine (DA), noradrenaline, 3,4-dihydroxyphenylglycol, serotonin (5-HT) and 5-hydroxyindoleacetic acid (HPLC/ED). Also there was no change in these monoamines and metabolites in the prefrontal cortex of Pb(2+) exposed rats. However, turnover of 5-HT in prefrontal cortex, as indicated by 5-hydroxytryptophan accumulation 30 min after acute treatment with the decarboxylase inhibitor NSD-1015 (100 mg/kg IP), was lower in the Pb(2+) exposed rats. In the striatum AMPH-induced (1 mg/kg IP) turnover of DA, evidenced as L-DOPA accumulation after NSD-1015, was increased to a lesser extent in the Pb(2+) exposed rats (P < 0.05). The nitric oxide synthase inhibitor 7-nitroindazole (10 mg/kg IP) attenuated the latter effect, indicating that neuronal NO mediates this AMPH effect, at least in part. Moreover, DA D(2) receptor sensitivity developed in Pb(2+) exposed rats, as evidenced by enhanced quinpirole-induced yawning activity and enhanced quinpirole-induced locomotor activity (each, P < 0.05). These findings indicate that ontogenetic exposure to lead can have consequences on monoaminergic neuronal function at an adult stage of life, generally promoting accentuated behavioral effects of direct and indirect monoaminergic agonists, and related to increased dopamine turnover in basal ganglia.