Lead acetate

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

Limitations of the lead acetate impregnated paper tape method for hydrogen sulfide.

Abstract: Field experience with the lead acetate impregnated paper tape sampler has indicated that large errors may arise in this method due to fading of the color of the precipitated lead sulfide spots. This fading is due to the action of light, sulfur dioxide, ozone, on other substances capable of oxidizing lead sulfide. The moisture content or relative humidity of the air sample must be maintained at an appropriate level to ensure reaction with the impregnated paper tape. The effects of the factors have been investigated in laboratory experiments with known concentrations of H2S. A number of antioxidants were studied in relation to the stability of the resultant spots to light and oxidation Orthophenyl phenol was found to be the most effective antioxidant for this purpose. A number of necessary precautions to be employed in the use of the lead acetate method are recommended and the limitations are discussed.

Effect of Lead Toxicity on Cytogenisity, Biochemical Constituents and Tissue Residue with Protective Role of Activated Charcoal and Casein in Male Rats

Abstract: Lead is a common industrial and environmental pollutant. Prolonged exposure of a sub- lethal dose to this toxicant is associated with oxidative stress, damage of DNA and considered to be a risk factor for kidney, liver added to many disorders. This study was carried out to investigate the most toxic effects of lead with trial to diminish this toxicity by supplementation of casein or activated charcoal. Therefore, forty mature male albino rats were used , they divided into four equal groups, 10 rats of each. Group 1 was considered as control. Rats of other groups (2, 3 and 4) were supplemented lead acetate at a dose of 0.5 g/100 ml drinking water for 2 months. Gr 3 is given charcoal at a concentration of 0.05g ration, while in Gr 4 casein is mixed with ration at a concentration of 20 g/100 g ration. Group 2 revealed significant increases in serum AST, ALT, ALP, LDH, GGT, TB, TC, LDL and CAT levels and decreased total protein, HLDL, VLDL, trace mineral salts, SOD and GSH- px. The results of haematological study evoked a significant decrease in the red blood cells (RBCs) count, blood haemoglobin (Hb) concentration and packed cell volume (PCV). Cytogenetic study resulted a significant increase in the percent of multinucleated polychromatic erythrocytes (MPCE) as well as significant increase in the polychromatic- erythrocytes (PCE) and normochromatic erythrocyte (NCE) ratio (PCER/NCE) Lead concentration in level serum and different tissues showed lead accumulation in serum, kidney, liver, muscle, intestine and spleen. Supplementation of charcoal and casein induce protective effects against lead toxicity in most of above parameter studies, and casein showed higher efficacy in the protection of lead- induced toxicity than charcoal.

Biochemical and molecular effects of gestational and lactational coexposure to lead and cadmium on ovarian steroidogenesis are associated with oxidative stress in f1 generation rats

Abstract: Few studies have characterized the molecular and biochemical mechanisms involved in ovarian steroidogenesis disruption by heavy metals, such as lead and cadmium coexposure, on F1 generation offspring. In this study, adult pregnant female rats were treated subcutaneously (0.05 mg/kg of body weight per day) with sodium acetate (control), lead acetate, and cadmium acetate separately and in combination throughout gestational and lactational period, and all animals from each of the experimental groups were sacrificed by decapitation on postnatal day 56 for various assays. The activities of key steroidogenic enzymes (17β-hydroxysteroid dehydrogenase and 3β-hydroxysteroid dehydrogenase) decreased in all the metal-treated groups. But the most significant decrease in the activities was observed in the cadmium-treated group, whereas the combined exposure group showed an intermediate effect. Serum estradiol and progesterone levels were also significantly altered in all the metal-treated groups, with the cadmium-exposed group showing maximum reductions as compared with the control group. The inhibitory effects of lead and cadmium on ovarian steroidogenic acute regulatory protein (StAR) mRNA levels along with CYP11 mRNA levels were also observed. Ovarian cholesterol content measured also showed significant depletion in all the metal-treated groups, with the cadmium-exposed group showing the maximum depletion. The activities of ovarian enzymatic antioxidants, such as superoxide dismutase, catalase, and glutathione peroxidase, were all significantly diminished along with significant depletion in nonenzymatic antioxidants. Lipid peroxidation was elevated significantly in all the metal-treated groups. In conclusion, lead and cadmium inhibit ovarian steroidogenesis by downregulating StAR gene expression along with inhibiting activities of steroidogenic enzymes and antioxidant system.

Exposure to a Low Lead Concentration Impairs Contractile Machinery in Rat Cardiac Muscle

Abstract: Lead exposure has been considered to be a risk factor for hypertension and cardiovascular disease. Our purpose was to evaluate the effects of low plasma lead concentration on cardiac contractility in isolated papillary muscles. Wistar rats were divided in control group or group treated with 100 ppm of lead acetate in the drinking water for 15 days. Blood pressure (BP) was measured weekly. At the end of the treatment period, the animals were anesthetized and euthanized, and parameters related to isolated papillary muscle contractility were recorded. The lead concentrations in the blood reached 12.3 ± 2 μg/dL. The BP was increased in the group treated with 100 ppm of lead acetate. Lead treatment did not alter force and time derivatives of the force of left ventricular papillary muscles. In addition, the inotropic response induced by an increase in the extracellular Ca2+ concentration was reduced in the Pb2+ group. However, the uptake of Ca2+ by the sarcoplasmic reticulum and the protein expression of SERCA and phospholamban remained unchanged. Postrest contraction was similar in the both groups, and tetanic peak and plateau tension were reduced in lead group. These results demonstrated that the reduction in the inotropic response to calcium does not appear to be caused by changes in the trans-sarcolemmal calcium flux but suggest that an impairment of the contractile machinery might be taking place. Our results demonstrate that even at a concentration below the limit considered to be safe, lead exerts deleterious effects on the cardiac contractile machinery.

Protective Effects of PGC-1α Against Lead-Induced Oxidative Stress and Energy Metabolism Dysfunction in Testis Sertoli Cells

Abstract: The reproductive system is sensitive to lead (Pb) toxicity, which has long been an area of research interest, but the underlying mechanisms remain to be illustrated. Peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α) is pivotal in mitochondrial function. In this study, mouse testis Sertoli cells (TM4 cells), PGC-1α lower-expression (PGC-1α(-)) TM4 cells and PGC-1α overexpression (PGC-1α(+)) TM4 cells were used to explore the protective roles of PGC-1α against lead toxicity on the mouse reproductive system. Lead acetate (PbAc) exposure decreased the expression level of PGC-1α, increased the intracellular level of reactive oxygen species (ROS), and reduced the level of ATP in the three TM4 cell lines. The effects of PbAc on intracellular ATP level and on ROS content were significantly weakened in PGC-1α(+)TM4 cells versus TM4 cells and were significantly amplified in PGC-1α(-)TM4 cells versus TM4 cells. These results suggest that PGC-1α is a protective factor against PbAc-induced oxidative stress and energy metabolism dysfunction in the mouse reproductive system, thereby holding the potential of being developed as a preventive or therapeutic strategy against disorders induced by lead exposure.