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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 correlation between acute and chronic treatments, and between cell and model membranes, suggests that the present observations may be relevant in the pathogenesis of lead intoxication in humans.
19 citations
TL;DR: Blood arsenic concentration and bioavailability decreased and lower absorption of As was observed when co-administered with Pb, suggesting other effects from physical and chemical parameters could contribute to the bioavailability of arsenic in complex real environmental samples.
Abstract: Arsenic (As) and lead (Pb) are common contaminants found in mine waste materials. For an evidence-based risk assessment, it is important to better understand the potential interaction of mixed contaminants; and this interaction study was investigated in an in vivo rat model. Following co-administration of a fixed dose of AsV as in sodium arsenate and different doses of Pb as lead acetate to Sprague–Dawley rats, blood arsenic concentration and bioavailability decreased. A decrease in As blood concentration when lead was co-administered was observed with increasing lead doses. Pharmacokinetic parameters for As in the blood showed faster absorption and elimination of this metalloid in the presence of Pb. The elimination half-life of As decreased from 67 days in As solo group to 27–30 with doses of Pb. Bioavailability of As was also decreased by 30–43 % in the presence of Pb. Decreased urinary excretion of Pb and tissue accumulation were also observed. It indicates lower absorption of As when co-administered with Pb. A probable explanation for these findings is that As co-administration with Pb could have resulted in the formation of less soluble lead arsenate. However, such an interaction between As and Pb could only explain about one-third of the variation when real mine waste materials containing both of these elements were administered to rats. This suggests that other effects from physical and chemical parameters could contribute to the bioavailability of arsenic in complex real environmental samples.
19 citations
TL;DR: The μ‐receptor binding contrasts with previously described impairment of antinociceptive effects of μ‐agonists suggesting that the toxicity is not manifested at the μ‐binding site, and the δ‐opioid receptor appears to be more sensitive to lead exposure, which may suggest irreversible damage in the production of the receptor protein.
Abstract: 1. Low level lead exposure has been shown to impair the development of opioid peptide levels in the brain, and to impair antinociceptive responses to opioid drugs. We have now studied the effects of lead exposure on the development of opioid receptors using ligand binding studies. 2. The ontogenesis of mu- and delta-opioid binding sites was studied using rat whole brain membranes and [3H]-[D-Ala2MePhe4-Gly-ol]enkephalin and [3H]-[D-Pen2,D-Pen5]enkephalin as binding ligands. Rats were exposed to lead during development by addition of lead acetate (at 100-1000 p.p.m.) to the maternal drinking water from conception to postnatal day 14. 3. Perinatal lead exposure had no significant effects on the binding affinity (KD) or binding capacity (Bmax) for the mu-opioid receptor measured at postnatal days 10, 21 and 30. Lead exposure (at 1000 p.p.m.) increased the KD for the delta-opioid receptor at postnatal days 15, 21, 35 and 50 but had no effect on the binding capacity. No indications of overt toxicity were observed and blood lead levels were in the ranges considered to represent subclinical lead toxicity in man. 4. The lack of effect of lead on mu-receptor binding contrasts with previously described impairment of antinociceptive effects of mu-agonists suggesting that the toxicity is not manifested at the mu-binding site. However, the delta-opioid receptor appears to be more sensitive to lead exposure and the persistent changes in delta-site affinity after cessation of lead exposure suggest irreversible damage in the production of the receptor protein.
19 citations
TL;DR: It is observed that lead acetate, as well as geraniol, can affect liver carboxylesterase activity, and this effect can reduce with Geraniol treatment.
Abstract: In this study, the effect of geraniol (50 mg/kg for 30 d), a natural antioxidant and repellent/antifeedant monoterpene, in a rat model of lead acetate-induced (500 ppm for 30 d) liver damage was evaluated. Hepatic malondialdehyde increased in the lead acetate group. Reduced glutathione unchanged, but glutathione S-transferase, glutathione reductase, as well as carboxylesterase activities decreased in geraniol, lead acetate and geraniol + lead acetate groups. 8-OhDG immunoreactivity, mononuclear cell infiltrations and hepatic lead concentration were lower in the geraniol + lead acetate group than the lead acetate group. Serum aspartate aminotransferase and alanine aminotransferase activities increased in the Pb acetate group. In conclusion, lead acetate causes oxidative and toxic damage in the liver and this effect can reduce with geraniol treatment. However, we first observed that lead acetate, as well as geraniol, can affect liver carboxylesterase activity.
19 citations
TL;DR: The behaviour of the treated offspring in social encounters was shown by ethological procedures to differ from that of controls and the behavioural effects of lead differed between males and females and were different in juveniles from those seen in adulthood.
19 citations