Lead acetate

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

Behavioral effects of chronic lead ingestion on laboratory rats.

Abstract: Rats contineously exposed to lead acetate solutions were tested on a visual discrimination reversal problem, on the open field and in 2 shuttle avoidance situations. High lead intake produced slower acquisition of the visual discrimination problem but had no effect on reversal performance. High lead intake reduced activity on the open field and improved performance on both shuttle avoidance problems. Results are interpreted to indicate that the effects produced by exposure to lead may involve an increase in responsiveness to aversive situations.

Effect of Ascorbic Acid and Thiamine Supplementation at Different Concentrations on Lead Toxicity in Liver

Abstract: Objective: To investigate the effect of ascorbic acid [vitamin C (VC)] on liver damage parameters in the lead-exposed mice, when given in combination with thiamine [vitamin B1 (VB1)] at different concentrations. Methods: Sixty-six male mice were randomly assigned into 11 groups (n 5 6). Mice in Group I were supplied with only the tap water as the drinking water; mice in Group II were provided with a tap water containing 0.2% lead acetate; mice in Group III–XI were given different dose of VC (140, 420, 1260 mg kg 21 bw) and VB1 (10, 30, 90 mg kg 21 bw) according to 3 3 3 factorial design by oral gavages, along with ingestion of 0.2% lead acetate. After 42 test days, DNA damage of liver cells was assessed using single-cell gel electrophoresis. The apoptosis rate of liver cells was determined by flow cytometry. The activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in blood and the level of reduced glutathione (GSH) in liver cells were measured based on individual biochemical reactions. Results: Compared with the Group I, sub-chronic lead ingestion (Group II) resulted in a significant decrease of Hb, GSH-PX, SOD in blood and GSH level in liver cells; lead exposure induced also a significant increase in DNA damage and apoptosis of liver cells (P < 0.05). Supplementation with VC and VB1, however, reversed these effects. The best effective combination was VC (420 mg kg 21 bw) and VB1 (10 mg kg 21 bw), followed by the combination of VC (420 mg kg 21 bw) and VB1 (30 mg kg 21 bw). But no reversion was shown in the combination of the highest combination of VC (1260 mg kg 21 ) and VB1 (90 mg kg 21 ). Conclusions: These findings strongly indicated that combination of VC and VB1 can lessen the damage to liver cells from oxidative stress induce by lead, but the antioxidant effects are dependent on their concentrations.

Mechanism of action of lead on neuromuscular junctions.

Abstract: Effects of bath-applied lead acetate on nerve-evoked and spontaneous neurotransmitter release were studied at the neuromuscular junction of the rat using conventional microelectrode recording techniques. Lead (20, 100 microM) depressed end-plate potential (EPP) amplitude within 5 min of application without affecting miniature end-plate potential (MEPP) amplitude. Increasing bath Ca2+ concentration from 2 mM to 4 or 8 mM caused a concentration-dependent reversal of lead-induced block of nerve-evoked EPPs. When lead was washed out of the bath, EPP amplitude either returned to control values, or was potentiated. Mean quantal content (m) was reduced significantly by lead treatment, an effect due primarily to a decrease in the immediately available store of transmitter (n). The probability of transmitter release (p) was either unchanged or slightly increased by lead. In contrast to its depressant effect on evoked transmitter release, spontaneous transmitter release, as measured by MEPP frequency, was increased by lead. MEPP frequency was increased from control levels of 1.2-3.2/sec to 12-16/sec by 100 microM lead. When lead was removed from the bath solution, MEPP frequency returned to control levels. Lead-induced increases in MEPP frequency still occurred when Ca2+ was removed from the external bath solution, or when 1 mM Mn2+ was added to block nerve terminal Ca2+ channels, suggesting that extracellular Ca2+ is not required for lead to increase spontaneous release. It is suggested that lead exerts actions at multiple sites at the presynaptic nerve terminal. An extracellular action of lead on transmitter release mechanisms is likely to be due to a competitive antagonism with Ca2+ for entry through Ca2+ channels. An intracellular action of lead is indicated by the depression of n, and the ability of lead to stimulate spontaneous acetylcholine release in the absence of external Ca2+ entry.

Lipid abnormalities in rats given small doses of lead

Abstract: Previous human and experimental studies have demonstrated that lead exposure may modify the metabolism of lipids. Several studies have indicated that exposure to lead produces an increase in lipid peroxidation and inhibits blood superoxide dismutase activity. Recently, lipid peroxides have been shown to impair tissue membranes and to be a risk factor for vascular diseases. The aim of the present investigation was to evaluate the impact of subclinical lead poisoning on rat lipids in the context of atherosclerosis. The degree of poisoning was analogous to that in populations exposed to lead in a contaminated environment. Experiments were performed on male Buffalo rats with body weights of 150–200 g. The experimental animals received lead acetate intragastrically in doses of 35 mg lead/kg body wt. (Pb/kg) once weekly or 70 mg Pb/kg twice weekly for 7 weeks. Control rats were fed in the same manner with sodium acetate equimolar to the acetate in the lead acetate solution. One day after the feeding was over, venous blood samples, under ether anesthesia, were collected. The animals were killed by exsanguination and the liver was excised for determination of the metal (lead, copper, and zinc) content. A segment of the abdominal aorta was excised for histological examination. In venous blood the following were estimated: triglycerides, total cholesterol, high-density lipoprotein (HDL)-cholesterol fraction, serum lipid peroxides, and blood superoxide dismutase activity. Metal content (lead, copper, and zinc) in blood and liver was determined by means of atomic absorption spectrophotometry. In rats poisoned with small doses of lead, decreases in the plasma cholesterol level and the HDL-cholesterol fraction were observed. In parallel with the decrease in the cholesterol concentration, lead increases the serum triglyceride level, this increase being dependent upon lead levels in blood. In our studies a significant influence of lead on serum lipid peroxide level or blood superoxide dismutase activity was not found. In the histological examination, atrophy of the elastic fibers in the aorta was observed. The possible significance of the inhibitory effect of lead on lipoprotein lipase activity is discussed.