Topic
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 present results showed that lead could induce toxicity in PC12 cells after 24 hours with as little as 1 μM in a concentration-dependent manner, which might mean lead could cause PC12 cell death, in which apoptosis or programmed cell death plays an important role.
Abstract: The nervous system is one of the most important targets of lead poisoning. Despite decades of study, the exact mechanism of lead toxicity has not been fully elucidated. One of the suggested mechanisms of lead toxicity is induction of apoptosis, which has not been shown yet in some neuronal cells such as pheochromocytoma cells (PC12). Therefore, the present study sought to examine the effect of lead poisoning on apoptosis in PC12 cells as a suitable model of neuronal cell study. The present results showed that lead could induce toxicity in PC12 cells after 24 hours with as little as 1 muM in a concentration-dependent manner. In Western blot analysis, the ratio of Bax/Bcl-2 protein expression in cells incubated with 3, 30, and 90 muM lead acetate significantly increased compared to controls. Additionally, a DNA laddering pattern in lead-treated cells was shown, which could indicate nuclear fragmentation. It might be concluded that lead could cause PC12 cell death, in which apoptosis or programmed cell death plays an important role.
25 citations
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TL;DR: It can be concluded that E. cottonii extracts could be a potent natural product and can provide a promising hepatoprotective effect against lead acetate-induced hepatotoxicity in mice.
Abstract: Background: Lead is one of the most toxic metals, producing severe organ damage in animals and humans. Oxidative stress is reported to play an important role in lead acetate-induced liver injury. Aim: This study was carried out to investigate the role of ethanol extract of Eucheuma cottonii in protecting against lead acetate-induced hepatotoxicity in male mice. Materials and Methods: The sample used fifty male mice which were divided into five groups: negative control (mice were given daily with Aquadest); positive control (mice were given daily with lead acetate 20 mg/kg body weight (BW) orally once in a day for 21 days); and the treatment group (mice were given E. cottonii extracts 200 mg, 400 mg, and 800 mg/kg BW orally once in a day for 25 days, and on the 4th day, were given lead acetate 20 mg/kg BW 1 h after E. cottonii extract administration for 21 days). On day 25, the levels of serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvate transaminase (SGPT), alkaline phosphatase (ALP), malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GPx) were measured. The data of SGOT, SGPT, ALP, MDA, SOD, and GPx were analyzed with one-way ANOVA, followed by least significant difference test. Results: The results showed that oral administration of lead acetate 20 mg/kg BW for 21 days resulted in a significant increase in SGOT, SGPT, ALP, and MDA levels. Moreover, there was a significant decrease in SOD and GPx levels. Treatment with E. cottonii extracts of 800 mg/kg BW but not with 200 mg/kg BW and 400 mg/kg BW significantly (P < 0.05) decreased the elevated SGPT, SGOT, ALP, and MDA levels as compared to positive control group. Treatment with E. cottonii extracts of 800 mg/kg BW also showed a significant increase in SOD and GPx levels as compared to positive control group. Treating mice with lead acetate showed different histopathological changes such as loss of the normal structure of hepatic cells, blood congestion, and fatty degeneration whereas animals treated with lead acetate and E. cottonii extracts showed an improvement in these changes and the tissue appeared with normal structures. Conclusion: It can be concluded that E. cottonii extracts could be a potent natural product and can provide a promising hepatoprotective effect against lead acetate-induced hepatotoxicity in mice.
25 citations
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TL;DR: The results indicate that two environmental contaminants have the ability to adversely affect NK cell cytotoxicity and the effects seen here with Pb and PCB on NK cells may in part explain the tumor inducing effect these chemicals are suspected of possessing via compromising the immune surveillance system.
25 citations
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25 citations
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TL;DR: The findings suggest that lead inhibits human sperm functions by reducing the levels of sperm intracellular cAMP, [Ca(2+)]i and tyrosine phosphorylation of sperm proteins in vitro.
Abstract: It is well known that there has been a worldwide decrease in human male fertility in recent years. One of the main factors affecting this is environmental pollution. Lead is one of the major heavy metal contaminants that threaten the health of animals and human beings in China. It preferentially accumulates in male reproductive organs and can be up to 10 µM in human seminal plasma. Lead impairs mammalian spermatogenesis and sperm quality in vivo. It also inhibits sperm functions in vitro but the underlying mechanisms remain unclear. Therefore, we aimed to investigate the in vitro toxicity of lead on human sperm functions and to elucidate the underlying mechanisms. Semen samples were collected from 20 healthy volunteers with different careers and backgrounds living in Nanchang, Jiangxi. Human sperm suspensions were treated with different concentrations of lead acetate (0, 0.5, 2.5, 10, 50, and 100 µM) and the viability, motility, capacitation and progesterone-induced acrosome reaction were examined. Treatment with 10-100 µM lead acetate dose-dependently inhibited total and progressive motility measures, capacitation and progesterone-induced acrosome reaction. It also dose-dependently decreased the intracellular concentrations of cyclic adenosine monophosphate (cAMP) and calcium ([Ca(2+)]i), and reduced the tyrosine phosphorylation of sperm proteins, all of which are thought to be key factors in the regulation of sperm function. Our findings suggest that lead inhibits human sperm functions by reducing the levels of sperm intracellular cAMP, [Ca(2+)]i and tyrosine phosphorylation of sperm proteins in vitro.
25 citations