Lead acetate

Abstract: Aqueous solutions of lead salts (1, 2) and saturated solutions of lead hydroxide (1) have been used as stains to enhance the electron-scattering properties of components of biological materials examined in the electron microscope. Saturated solutions of lead hydroxide (1), while staining more intensely than either lead acetate or monobasic lead acetate (l , 2), form insoluble lead carbonate upon exposure to air. The avoidance of such precipitates which contaminate surfaces of sections during staining has been the stimulus for the development of elaborate procedures for exclusion of air or carbon dioxide (3, 4). Several modifications of Watson's lead hydroxide stain (1) have recently appeared (5-7). All utilize relatively high pH (approximately 12) and one contains small amounts of tartrate (6), a relatively weak complexing agent (8), in addition to lead. These modified lead stains are less liable to contaminate the surface of the section with precipitated stain products. The stain reported here differs from previous alkaline lead stains in that the chelating agent, citrate, is in sufficient excess to sequester all lead present. Lead citrate, soluble in high concentrations in basic solutions, is a chelate compound with an apparent association constant (log Ka) between ligand and lead ion of 6.5 (9). Tissue binding sites, presumably organophosphates, and other anionic species present in biological components following fixation, dehydration, and plastic embedding apparently have a greater affinity for this cation than lead citrate inasmuch as cellular and extracellular structures in the section sequester lead from the staining solution. Alkaline lead citrate solutions are less likely to contaminate sections, as no precipitates form when droplets of fresh staining solution are exposed to air for periods of up to 30 minutes. The resultant staining of the sections is of high intensity in sections of Aralditeor Epon-embedded material. Cytoplasmic membranes, ribosomes, glycogen, and nuclear material are stained (Figs. 1 to 3). STAIN SOLUTION: Lead citrate is prepared by

Abstract: Lead exposure related oxidative stress has been incriminated, at least in part, to its toxic effects in different organs. The present investigation was carried out to study the ameliorative effects of antioxidant (ascorbic acid, alpha tocopherol or L-methionine) alone and antioxidant (alpha tocopherol) plus a conventional chelator (CaNa2 EDTA) on some of the parameters indicative of oxidative stress in the liver, kidney and brain in lead-exposed rats. Rats were given 0 (n=6, healthy controls) or 1 mg of Pb(2+)/kg b.w (n=30) as lead acetate solution in sterile normal saline ip for a period of 4 weeks. The ip injections were then withdrawn and lead exposed rats were randomly divided into five equal groups. Six lead-exposed rats were given no treatment during the 5th week (Pb group) to serve as positive controls. The rest four groups received either ascorbic acid, alpha tocopherol or L-methionine in the 5th week at the daily dose of 100 mg/kg b.w orally or alpha tocopherol as above plus CaNa2 EDTA at the rate of 110 mg/kg b.w twice a day ip for a period of 4 days. All the animals were sacrificed 1 day after the end of the experiment, and the liver, kidney and brain were quickly excised for the estimation of lead burden and alteration in the oxidative indices. Lead exposure for a period of 4 weeks followed by a period of 1 week to recover, resulted in significantly (P<0.05) higher accumulation of lead, associated with significant (P<0.05) increases in lipid peroxide level in the liver and brain, and non-protein bound thiol contents in the brain. Changes in the superoxide dismutase and catalase activities in lead-exposed rats did not reach statistical (P<0.05) significance. Treatment with antioxidants alone resulted in reversal of oxidative stress without significant decline in tissue lead burden. Tissue specific changes, following lead exposure and responses to the treatment with different antioxidants were recorded in the parameters of oxidative damage viz. lipid peroxide level, antioxidant enzymes and thiol contents.

Abstract: Curcumin, the major constituent of turmeric is a known, naturally occurring antioxidant. The present study examined the ability of this compound to protect against lead-induced damage to hippocampal cells of male Wistar rats, as well as lipid peroxidation induced by lead and cadmium in rat brain homogenate. The thiobarbituric assay (TBA) was used to measure the extent of lipid peroxidation induced by lead and cadmium in rat brain homogenate. The results show that curcumin significantly protects against lipid peroxidation induced by both these toxic metals. Coronal brain sections of rats injected intraperitoneally with lead acetate (20 mg/kg) in the presence and absence of curcumin (30 mg/kg) were compared microscopically to determine the extent of lead-induced damage to the cells in the hippocampal CA1 and CA3 regions, and to establish the capacity of curcumin to prevent such damage. Lead-induced damage to the neurons was significantly curtailed in the rats injected with curcumin. Possible chelation of lead and cadmium by curcumin as its mechanism of neuroprotection against such heavy metal insult to the brain was investigated using electrochemical, ultraviolet spectrophotometric and infrared spectroscopic analyses. The results of the study show that there is an interaction between curcumin and both cadmium and lead, with the possible formation of a complex between the metal and this ligand. These results imply that curcumin could be used therapeutically to chelate these toxic metals, thus potentially reducing their neurotoxicity and tissue damage.

Abstract: The effects of lead ingestion on parameters indicative of copper status, and particularly on the activity of the copper-dependent metalloenzyme superoxide dismutase (SOD) in erythrocytes, were investigated in weanling and neonatal rats. In a series of experiments, Sprague-Dawley or Long-Evans rats were fed a nutritionally adequate purified diet (AIN-'76). Lead acetate was given orally in the drinking water (0, 100, 250, or 500 ppm Pb) to groups of 23 to 26-day-old rats for 5 weeks or intragastrically (0, 5, 11, 22, or 45 mg Pb/kg body wt/day) to pups from postnatal Days 2 through 20. Lead ingestion (250 and 500 ppm Pb) by weanling rats resulted in decreased concentrations of copper in blood (erythrocytes and serum), liver, and spleen, in increased concentrations of iron in liver and spleen, in increased spleen weight, and in a small decrease in hemoglobin and hematocrit values. There was a significant decrease in the activities of the copper metalloproteins erythrocyte superoxide dismutase (SOD) and serum ceruloplasmin (Cp). In contrast, in the neonate we found no significant effects of lead on copper concentrations in blood or tissue or on other measures indicative of copper status. Despite high blood lead concentrations (1-3 micrograms/ml), SOD activity was not decreased in the neonatal rat. In addition, lead had no direct effect in vitro on the activity of bovine blood superoxide dismutase. On the basis of both the in vitro and in vivo studies, it appears likely that the observed decrease in SOD in young rats is caused indirectly by a lead-induced copper deficiency rather than by a direct inhibitory effect of lead.

Abstract: This study examined whether lead-induced alterations in selected parameters that are indicative of oxidative stress accompany the toxic effects of lead in red blood cells (RBCs) in vivo. It also explored the possibility that treatment with N-acetylcysteine (NAC) or succimer (meso-2,3-dimercaptosuccinic acid) was capable of reversing parameters indicative of lead-induced oxidative stress. Fisher 344 rats were given 2000 ppm lead acetate in their drinking water for 5 weeks. The lead was then removed and the animals were given NAC (800 mg/kg/day) or succimer (90 mg/kg/day) in their drinking water for 1 week, after which the RBCs were harvested. Animals not given lead and those given lead, but not NAC or succimer, served as negative and positive controls, respectively. At the end of the experiment, blood-lead levels were 35 +/- 4 microg/dl in lead-treated animals, which were reduced to 2.5 +/- 1 microg/dl by treatment with succimer and to 25 +/- 3 microg/dl by treatment with NAC. Lead-exposed animals demonstrated signs of anemia as evidenced by anisocytosis, poikilocytosis, and alterations in hemoglobin, hematocrit, and mean corpuscular volume. Lipid peroxidation, as evidenced by increased malondialdehyde (MDA) content, as well as decreases in reduced glutathione (GSH) and increases in catalase and glucose 6-phosphate dehydrogenase (G6PD) activity were noted in RBCs from lead-treated rats, suggesting that the lead induced oxidative stress. In addition, a significant reduction in blood delta-aminolevulinic acid dehydratase (ALAD) activity suggested that accumulation and autooxidation of delta-aminolevulinic acid might contribute to lead-induced oxidative stress. Treatment with either NAC or succimer reversed lead-induced alterations in MDA and GSH content, but only succimer appeared to partially restore ALAD activity. These results provide in vivo evidence supporting the hypothesis that lead induces oxidative stress in RBCs, which is reversible by treatment with a thiol antioxidant (NAC), as well as a chelating agent (succimer).