Lead acetate

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

Lead absorption and excretion in rats given insoluble salts of pectin and alginate.

Abstract: Exposure to environmental lead remains a widespread problem in most industrialized countries. Usage of modern agents purposed for elimination of heavy metals as well as for therapy and prevention of chronic poisoning does frequently result in toxic signs. Dietary nonstarch polysaccharides were suggested to be effective when used for this purpose. The present study was conducted to estimate metal binding capacity and effects of calcium salts of pectate and alginate on lead absorption, distribution, and removal with feces. Under in vitro conditions calcium alginate showed the highest lead-binding capacity in comparison with other agents studied. Metal binding capacity of calcium pectate was slightly lower. In rats simultaneous administration of lead acetate and suspensions containing calcium alginate or calcium pectate prevented metal absorption and significantly reduced lead accumulation in inner organs and femur. In experiments estimating lead removal from inner organs and femur in rats preliminary exposed to the heavy metal, calcium alginate and calcium pectate were the most effective agents studied in comparison with others, as indicated by reduced lead concentration in organs and femur as well as increased metal content in feces of laboratory animals. The results suggest that calcium pectate and calcium alginate may be considered perspective dietary compounds purposed for prevention and treatment of chronic lead poisoning.

Neoplasia induced in male rats fed lead acetate, ethyl urea, and sodium nitrite.

Abstract: Sprague-Dawley rats were exposed to 0, 26, or 2600 ppm lead as lead acetate in drinking water for 76 weeks. At 28 weeks of lead exposure, a portion of each group was exposed simultaneously to 6.36 g/kg ethyl urea (EU) and 2.0 g/kg sodium nitrite (NaNO2) for a duration of 20 weeks, and then continued an additional 28 weeks on standard diet free of EU and NaNO2. The animals were observed for incidence, latency, and distribution of tumors. Rats exposed to 2600 ppm lead alone had 81% renal tumors, while rats given 2600 ppm lead in combination with EU/NaNO2 had a 50% incidence. Renal tumors did not occur in the EU/NaNO2 only or EU/NaNO2-26 ppm lead groups. The major tumor type found in EU/NaNO2-exposed rats was lymphosarcoma. Lead did not appear to be syncarcinogenic to the activity of ethylnitrosourea, the carcinogen formed by oral exposure to EU and NaNO2. The lead-induced renal neoplasms were histologically similar to those which occur spontaneously in man and, therefore, may serve as an animal model to study human disease.

Silymarin and dimercaptosuccinic acid ameliorate lead-induced nephrotoxicity and genotoxicity in rats.

Abstract: We studied the effect of silymarin and dimercaptosuccinic acid (DMSA), a chelating agent that was administered individually or in combination against lead (Pb) toxicity in rats. Wistar rats (200 ± 20) were randomly divided into five groups. Group A served as a control. Groups B-E were exposed to 2000 ppm of lead acetate in drinking water for 8 weeks. Group B served as a positive control. Group C received silymarin (100 mg kg(-1) orally) for 8 weeks. Group D received DMSA (75 mg kg(-1) orally) once daily for the last 5 days of treatment. Group E received DMSA and silymarin as groups C and D, respectively. The effect of Pb was evaluated and accordingly the treatments on blood lead levels (BLLs), renal system, and genotoxic effects were calculated using comet assay. The BLLs were significantly increased following the exposition of lead acetate. The administration of silymarin and DMSA provided reduction in BLLs. Silymarin and DMSA provided significant protection on the genotoxic effect of Pb. The toxic effect of Pb on kidneys was also studied. Our data suggest that silymarin and DMSA improve the renal histopathological lesions.