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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: Methionine may be useful as a supportive therapy in chelation of Pb, useful in chelating Pb and counter-acting the toxic effects, as evidenced by restoration of the Pb-induced decrease in hepatic GSH level by treatment with methionine.
15 citations
15 citations
TL;DR: RT has a beneficial impact on lead-induced toxicity due to its scavenging and antioxidant effect in rats, and is known to have powerful antioxidant activity that could play a protective role in oxidative stress-mediated diseases.
Abstract: Flavonoids are known to have powerful antioxidant activity that could play a protective role in oxidative stress-mediated diseases. Rutin (RT) is a flavonol glycoside composed of the flavonol quercetin and disaccharide rutinose. The protective effect of RT against nephrotoxicity induced by lead acetate was evaluated. Male albino rats of Wistar strain were used in this study. Animals were given lead acetate after a week of pretreatment with RT (50 mg/animal/day). Lead acetate exposure resulted in an increase in the uric acid, creatinine (CRN) and blood urea nitrogen (BUN) levels and a decrease in glutathione, superoxide dismutase, catalase and glutathione peroxidase (GPx) activities. Lead acetate treatment decreased GSH levels by 2-fold and the activities of GSH metabolizing enzymes decreased to a range of 2–2.5-fold in renal tissue (p < 0.05). These changes were reversed significantly in animals receiving pretreatment of RT. Treatment of rats with RT prior to the treatment with lead resulted in th...
15 citations
TL;DR: Differences in evolution are more likely related to differences in the development of resistance of the cerebral capillary to lead, or in the efflux of lead, rather than to the blood lead concentrations.
Abstract: Lead encephalopathy was produced in immature Sprague-Dawley rats with an intraperitoneal (IP) injection of 60 µg/g body weight of lead acetate administered daily from the fifth day after birth. Macroscopic and light microscopic study of the nervous system, estimations of the blood-brain barrier permeability to proteins and brain water content were performed every two days thereafter. Lead levels in total blood, plasma, and several brain areas were measured at the same intervals by flameless atomic absorption spectrometry. Electron microscopic study of the cerebellum was done 2, 6, and 12 days after beginning lead administration. After two days of lead administration and before any pathological change occurred the increase in lead level was greater in the cerebellum than in other brain areas. After four to six days, hemorrhagic lead encephalopathy developed and was most prominent in regions with higher lead levels. From day 11 to 14, there were two possible courses: a) improvement of the clinical status and morphological findings in 25% of the animals, or b) progression of abnormal clinical signs and death. Cerebral edema, both intra- and extracellular, may have contributed to the fatal evolution. The mechanism of this edema appeared complex and may have involved resorption failure. Good correlations were observed among progression of the clinical signs, high water content in the brain, morphological evidence of cerebral edema, and a high cerebellar lead level. In contrast, high blood lead levels could be associated with clinical improvement, normal brain water content, and regression of the pathological findings. These data suggest that differences in evolution are more likely related to differences in the development of resistance of the cerebral capillary to lead, or in the efflux of lead, rather than to the blood lead concentrations
15 citations
TL;DR: It is found that poisoning with lead and its accumulation at doses of 50 and 100 ppm in femoral bone marrow of rats decreased the expression of the collagen type II and osteocalcin genes in MSCs and in the chondrogenic and osteogenic media, respectively.
Abstract: Background: Lead is one of the sustainable metals with devastating effects on many tissues. This study, examined the adverse effect of lead poisoning on the gene expression of collagen type II and osteocalcin by mesenchymal stem cells (MSCs) cultured in chondrogenic and osteogenic media, respectively. Methods: We used 18 male Wistar rats, divided in 3 groups. In addition to libitum feed as the control, treatment I and treatment II groups were fed by distilled water, distilled water with a dose of 50 ppm lead acetate II and distilled water with a dose of 100 ppm lead acetate II, respectively, over a 2-month period. The MSCs of rat femur were isolated in DMEM medium. After the second passage, the media were replaced separately with chondrogenic and osteogenic media over another 21 days. Then, Collagen Type II and Osteocalcin genes expression were investigated by real time PCR. Results: Collagen Type II and Osteocalcin genes expression in treatments I and II groups showed meaningful decreases compared with that of the control group. Also, the concentration of collagen type II in treatment II group in chondrogenic medium was significantly reduced compared with Osteocalcin concentration in osteogenic medium. Conclusion: We found that poisoning with lead and its accumulation at doses of 50 and 100 ppm in femoral bone marrow of rats decreased the expression of the collagen type II and osteocalcin genes in MSCs and in the chondrogenic and osteogenic media, respectively.
15 citations