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Lead acetate
About: Lead acetate is a research topic. Over the lifetime, 2636 publications have been published within this topic receiving 69739 citations.
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TL;DR: The use of barley phenolic compounds were successive to ameliorate the toxic effects of lead acetate, as reflected in the decreased levels of lipid peroxidation marker and the increased antioxidant activity.
Abstract: This study was conducted to explore the effects of lead acetate and barley phenolic compounds, alone or in combination, on lipid peroxidation marker and some antioxidant enzymes using a rabbit model. Rabbits were provided with drinking water containing lead acetate (500 ppm) and/or gastro-gavaged with barley phenolic compounds (250 mg/kg/day) for 30 days. Following overnight fasting, the animals were sacrificed, and the levels of glutathione and malondialdehyde and the activities of glutathione S-transferase and glutathione peroxidase in brain, liver and kidney tissues were measured spectrophotometrically. Treatment with lead acetate significantly decreased the activities of glutathione S-transferase, glutathione peroxidase and the level of reduced glutathione, and it significantly increased the level of lipid peroxidation marker. Conversely, treatment with barley phenolic compounds, whether alone or in combination with lead acetate, significantly increased the activity of antioxidant enzymes and the level of reduced glutathione, and significantly decreased the level of lipid peroxidation marker. The use of barley phenolic compounds were successive to ameliorate the toxic effects of lead acetate, as reflected in the decreased levels of lipid peroxidation marker and the increased antioxidant activity.
14 citations
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TL;DR: It is evident that lead acetate is a weak mutagen, whereas the use of mercury needs more cautions.
Abstract: The effects of two heavy metal compounds viz., lead acetate and mercuric chloride were studied on the polytene chromosomes in Anopheles stephensi. Various chromotoxic effects such as inversions, translocations, and breaks were observed. In the larvae treated with lead acetate, an increased incidence (as compared to controls) of asynapsis in the X-chromosome was also observed. From the present studies, it is evident that lead acetate is a weak mutagen, whereas the use of mercury needs more cautions.
14 citations
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TL;DR: Co-administration of aqueous Moringa extract with lead significantly alleviated lead-induced adverse effects and restored the lead perturbations through reduction of oxidative stress–induced DNA damage via amelioration of NF-kB and TNF-α which kept hepatocyte integrity and reduced serum hepatic enzyme activities.
Abstract: Current research was performed to explore the hepatoprotective potential of Moringa oleifera leaves extract on lead acetate–induced hepatic injury. Twenty-four male Wistar rats were divided equally into 4 groups. The first group was control, while the second, third, and fourth groups were given 200 mg/kg aqueous Moringa extract only, 100 mg/kg lead only, and 100 mg/kg lead plus 200 mg/kg aqueous Moringa leaves extract, respectively, via oral gavage for 4 weeks. Weight gain and feed efficiency ratio were recorded. Serum lipid profiles, liver enzyme activities, and proteins beside hepatic superoxide dismutase activity, reduced glutathione, tumor necrosis factor alpha (TNF-α), and deoxyribonucleic acid fragmentation were assessed. Liver histopathological examination and nuclear factor kappa B (NF-kB) immunohistochemistry were performed. Administration of lead lowered (P < 0.05) weight gain, feed efficiency ratio, and perturbed lipid profile than control. Lead increased liver enzyme activities and TNF-α, while reduced serum proteins and hepatic antioxidant markers compared to control. Lead aggravated hepatic DNA fragmentation beside the presence of histopathological lesions. Co-administration of aqueous Moringa extract with lead significantly alleviated lead-induced adverse effects. The administration of aqueous Moringa extract with its antioxidant significantly restored the lead perturbations through reduction of oxidative stress–induced DNA damage via amelioration of NF-kB and TNF-α which kept hepatocyte integrity and reduced serum hepatic enzyme activities.
14 citations
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TL;DR: Airways are the primary target of lead exposure from atmospheric pollution, its effect on airway smooth muscle and their responsiveness to bronchoactive agents is not clearly understood and the involvement of airway epithelium was examined.
Abstract: Airways are the primary target of lead exposure from atmospheric pollution, its effect on airway smooth muscle and their responsiveness to bronchoactive agents is not clearly understood. In the present investigation the effect of lead on the isolated airway smooth muscle activity was studied in organ bath set-up. Further the involvement of airway epithelium was examined and the responsiveness of airway smooth muscle to adenosine, acetylcholine (bronchoconstrictors) and isoproterenol (bronchodilator) was also investigated. Lead in concentration of 10(-12) M to 10(-4) M produced concentration-dependant contractile response in rat tracheal rings. Acetylcholine and adenosine induced concentration-dependent contractile response was slightly inhibited after lead exposure. The relaxant response to isoproterenol was also inhibited in lead exposed tissues. Epithelium removal did not significantly change the contractile response to lead suggesting that the lead induced contraction of airway smooth muscle is epithelium independent.
14 citations
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TL;DR: Evaluated the ameliorative effects of curcumin on Pb‐induced hepatorenal toxicity in a rat model and found it to have antioxidative properties.
Abstract: Introduction Lead (Pb) is a ubiquitous toxic heavy metal that inflicts numerous clinical consequences on humans. Curcumin is the principal component of turmeric, which is reported to have antioxidative properties. This study aimed at evaluating the ameliorative effects of curcumin on Pb-induced hepatorenal toxicity in a rat model. Methods Thirty-six male Sprague-Dawley rats were randomly assigned into five groups with 12 rats in the control (normal saline) and six rats each for the lead-treated group (LTG) (50 mg/kg lead acetate [Pb acetate] for 4 weeks), recovery group (50 mg/kg Pb acetate for 4 weeks and left with no treatment for another 4 weeks), treatment group 1 (Cur100) (50 mg/kg Pb acetate for 4 weeks, followed by 100 mg/kg curcumin for 4 weeks), and treatment group 2 (Cur200) (50 mg/kg Pb acetate for 4 weeks, followed by 200 mg/kg curcumin for 4 weeks). All the experimental groups received oral treatments via orogastric-tube on alternate days. Pb concentration in the liver and kidney of the rats were evaluated using inductive-coupled plasma mass spectrometry techniques. Results Pb-administered rats revealed significant alteration in oxidative status and increased Pb concentration in their liver and kidney with obvious reduction of hemogram and increased in leukogram as well as aberration in histological architecture of the liver and kidney. However, treatment with curcumin reduces the tissue Pb concentrations and ameliorates the above mention alterations. Conclusions The results in this study suggested that curcumin attenuates Pb-induced hepatorenal toxicity via chelating activity and inhibition of oxidative stress.
14 citations