Lead acetate

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

Attenuation of lead-induced oxidative stress in rat brain, liver, kidney and blood of male Wistar rats by Moringa oleifera seed powder.

Abstract: Moringa oleifera is a tree belonging to Moringaceae family and its leaves and seeds are reported to have ameliorative effects against metal toxicity. In the present investigation, M. oleifera seed powder was tested against lead-induced oxidative stress and compared against meso-2, 3-dimercaptosuccinic acid (DMSA) treatment. Male Wistar rats (100-120 g) were divided into four groups: control (2000 ppm of sodium acetate for 2 weeks), exposed (2000 ppm of lead acetate for 2 weeks), Moringa treated (500 mg/kg for 7 days after lead exposure), and DMSA treated (90 mg/kg for 7 days after lead exposure). After exposure and treatment periods, rats were sacrificed and the brain was separated into cerebellum, hippocampus, frontal cortex, and brain stem; liver, kidney, and blood were also collected. The data indicated a significant (p<0.05) increase in reactive oxygen species (ROS), lipid perioxidation products (LPP), total protein carbonyl content (TPCC), and metal content of brain regions, liver, and kidney in the exposed group compared with their respective controls. In the blood, delta-amino levulinic acid dehydratase (ALAD) activity, RBC, WBC, hemoglobin, and hematocrit showed significant (p<0.05) decrease on lead exposure. However, administration of M. oleifera restored all the parameters back to control, tissue-specifically, and also showed improvement in restoration better than DMSA treatment, indicating reduction of the negative effects of lead-induced oxidative stress.

The effect of lead acetate toxicity on experimental male albino rat.

Abstract: The toxic effect of Pb ion (lead acetate) was investigated using male albino rats, which was ingested at 1/20, 1/40, and 1/60 sublethal doses. Relative to normal control, the ingestion of Pb(2+) induced significant stimulation in ALT and AST activity. In addition, total soluble protein and albumin contents of plasma were decreased, while the content of globulin was changed by the Pb(2+) treatments. The cholinesterase activity was inhibited, but the activities of alkaline and acid phosphates as well as lactate dehydrogenase were stimulated as a result of lead acetate intoxication. These observations were gradually paralleled across the experiment dose of the three doses of intoxicated Pb(2+). In the case of blood picture, Pb(2+) ingestion significantly reduced the contents of hemoglobin and RBC count of intoxicated rat's blood, while the plasma levels of T3 and T4 and blood WBC count were insignificantly decreased or unchanged. All results of the present study showed that the Pb(2+) ingestion was more effective in the case of the high dose (1/20 LD(50)) than that of the low dose (1/60 LD(50)) ingestion relative to the normal healthy control. The results of the present work advice the need to avoid exposure of humans to the lead compound to avoid injurious hazard risk.

Eight nerve in experimental lead poisoning.

Abstract: Forty healthy guinea pigs were poisoned with repeated peritoneal injections of lead acetate. After 7 weeks the animals were sacrificed and the inner ear with VIII nerve were examined histologically. The lead level in the blood was estimated in all animals after poisoning and in 10 healthy guinea pigs (control group). The sensory cells of the inner ear, the spiral and vestibular ganglion cells appeared to be normal. The VIII nerve in the majority of poisoned animals showed segmental deniyelina-tion and axonal degeneration. Theories on etiology and pathogenesis of the neuropathological changes in lead poisoning are discussed.

In vitro effect of lead acetate on human erythropoietic progenitors.

Abstract: Lead is known to induce hematological disturbances resulting from abnormalities in cell differentiation and hemoglobin synthesis during hematopoiesis. The aim of the present work was to study human erythropoiesis in vitro in the presence of lead. Human erythroblastic progenitors, burst-forming units-erythroid (BFU-E), were exposed to lead acetate at increasing concentrations during 14 days of culture. Hematotoxicity was evaluated in vitro according to proliferation and differentiation of cell colonies arising from BFU-E development. The ability of cells to synthesize proteins, porphyrins, and hemoglobin was measured by spectrophotometric tests and by high-pressure liquid chromatography (HPLC). Results showed that in the presence of 10(-3) mol/L lead acetate, no hemoglobinized cells were observed in culture and no fluorescent porphyrins were detected in cells. Up to 10(-3) mol/L, lead acetate is not cytotoxic, i.e., it does not induce cell destruction. The present work demonstrates that lead acetate interferes with the porphyrin synthesis of human erythroblastic progenitors in vitro. The decrease of porphyrin content with 10(-5) mol/L lead acetate suggest that delta-aminolevulinic acid dehydratase can be inhibited by lead acetate during in vitro erythropoiesis. In vivo erythropoiesis occurs in the bone marrow. As about 95% of the body burden of lead in adults is located in the bones with a biological half-life of some years, the concentration of lead acetate found to block porphyrin synthesis in vitro has to be compared with in situ bone marrow lead concentrations.