Lead acetate

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

Basic Lead Acetate: Promoting Effect on the Development of Renal Tubular Cell Tumors in Rats Treated With N-Ethyl-N-hydroxyethylnitrosamine

Abstract: The development of renal tubular cell tumors by the end of experimental week 32 was studied in inbred Wistar male rats fed a diet containing 1,000 or 500 ppm N-ethyl-N-hydroxyethylnitrosamine (EHEN) for 2 weeks and then given 1,00 ppm basic lead acetate (LA) for 20 weeks. A low dose of LA enhanced the development of renal tubular cell tumors in rats treated with EHEN and increased the number and size of the tumors. The incidence of renal tubular cell tumors at the end of week 32 was 50% in rats treated with 1,000 ppm EHEN for 2 weeks and 100% in rats treated with 1,000 ppm EHEN for 2 weeks and then given 1,000 ppm LA for 20 weeks. The incidences of renal tumors of more than 3 mm in diameter were 70% in rats treated with 1,000 ppm EHEN plus LA and 0% in rats treated with EHEN or LA alone. The low dose of LA showed the enhancing effect of the development of renal tubular cell tumors in rats treated with a subthreshold dose of 500 ppm EHEN.

HIGHLIGHTS Effect of Lead Acetate on Nitrite Production by Murine Brain Endothelial Cell Cultures

Abstract: One of the mechanisms by which lead may cause a perturbation in the nervous system is the alteration of endothelial cell function. This study investigated the effect of lead acetate on constitutive and cytokine-induced production of nitrite, a marker of nitric oxide, in brain microvascular endothelial cells. Nitric oxide synthase may be a target for lead and changes in its function can result in a cascade of physiological effects seen in vivo. Concentrations of 10, 100, and 1000 nM lead acetate, in the presence or absence of 100 ng lipopolysaccharide/ml, 400 U interferon-gamma/ml and 100 U tumor necrosis factor-alpha/ml, were added to confluent cultures of brain microvascular endothelial cells. Concentrations of lead acetate as low as 10 nM decreased constitutive levels of nitrite by 50% without inhibiting the inducible levels. Addition of 1 microM lead acetate had no effect on [3H]L-leucine incorporation, lactate dehydrogenase release, or cellular morphology, indicating that the effect was selective. Increasing the concentration of extracellular calcium to 2 mM abolished the inhibitory effect of lead acetate on the constitutive production of nitrite. These studies suggest that low concentrations of lead are capable of inhibiting nitrite produced by the calcium-dependent constitutive form of nitric oxide synthase while the calcium-independent, inducible form of nitric oxide synthase is not affected. These data provide another testable hypothesis for the as yet undetermined mechanisms of lead neurotoxicity.

Oxidative damage and OGG1 expression induced by a combined effect of titanium dioxide nanoparticles and lead acetate in human hepatocytes

Abstract: Titanium dioxide (TiO2) is a widely used nanomaterial that can cause biological damage through oxidative stress. At low concentrations, TiO2 can interact with lead acetate (PbAc) to produce different toxic responses, compared with TiO2 or PbAc alone. In this study, we utilized the following as indicators of toxic responses in human embryo hepatocytes (L02): reactive oxygen species (ROS), reduced glutathione (GSH), superoxide dismutase (SOD), and the DNA adducts 8-hydroxydeoxyguanosine (8-OHdG) and 8-oxoguanine DNA glycosylase homolog 1 (OGG1). These were used to evaluate the oxidative stress of TiO2 (at 0.001, 0.01, 0.1, 1, and 10 μg mL−1) mixed with PbAc (1 μg mL−1) on L02 cells without photoactivation. Compared with the negative control (1‰ dimethyl sulfoxide), TiO2 mixed with PbAc induced increased release of ROS (at 0.001, 0.01, 0.1, 1, 10 μg mL−1 TiO2), intracellular SOD activity (at 0.1 and 0.01 μg mL−1 TiO2), GSH levels (at 0.01–1 μg mL−1 TiO2), 8-OHdG levels (at 1 and 10 μg mL−1 TiO2), OGG1 expression (at 0.001–1 μg mL−1 TiO2), and cytotoxicity (at 0.1, 1, and 10 μg mL−1 TiO2) in L02 cells. There were no significant changes in ROS, GSH, SOD, 8-OHdG, or OGG1 levels when L02 cells were treated with TiO2 alone or PbAc alone. These findings indicate that TiO2 and PbAc in combination induce cytotoxicity and oxidative stress in L02 cells in the absence of photoactivation. © 2011 Wiley Periodicals, Inc. Environ Toxicol, 2012.

Abnormalities of erythrocytes and renal tubules of chicks poisoned with lead.

Abstract: Lead toxicosis was produced in chicks by feeding lead (as lead acetate) at the dose level of 5000 or 10,000 ppm. Signs of toxicosis included ataxia and decrease in body weight gain and feed intake. The lead content of livers of chicks fed the large dose (10,000 ppm) was 82.5 ppm and of controls, 0.5 ppm. In studies by light and electron microscopy various stages of mitosis were observed in the erythrocytes in the peripheral blood of chicks fed either dose. By light microscopy, necrosis of the epithelium of the proximal convoluted tubules of the kidneys was observed, and by electron microscopy, nuclei of these cells were seen to contain irregular-shaped, electron-dense inclusions.

Effects of sub-lethal exposure of lead acetate on histopathology of gills, liver, kidney and muscle and its accumulation in these organs of Clarias gariepinus

Abstract: The aim of this work was to study the effects of sub-lethal exposure of lead acetate on the histopathology of the gills, liver, kidney and muscle and its accumulation in these organs of Clarias gariepinus. Results showed that lead accumulation in the tissues of C. gariepinus was dependent on the exposure period and lead concentration. Gills and liver were the predominant storage tissue and the order of accumulation in tissues was gill > liver > kidney > muscle. Some structural changes were observed in different organs, especially in the gills of the fishes exposed to lead acetate. Epithelial hypertrophy and epithelial lifting were apparent in the gills of exposed fishes. The degeneration of cytoplasm and secondary lamellae was also observed. Necrosis of hepatocytes was apparent. Glomerular expansion and gaps between the muscular bundles were found in the fishes exposed to lead acetate.