Lead acetate

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

Lead acetate genotoxicity in suckling rats

Abstract: The mutagenic and carcinogenic potentials of lead are still being investigated. The aim of this study was to evaluate the genotoxic effect of lead acetate in the early period of life, when the organism is extremely sensitive to toxic effects of lead. Six-day-old suckling Wistar rats were exposed to lead (as acetate) either orally for 9 days (daily dose 2 mg Pb/kg b. wt., 18 mg/kg b.wt. total dose) or by a single intraperitoneal injection (5 mg Pb/kg b. wt.). DNA damage was investigated using the comet assay and in vivo micronucleus test. The results of the comet assay showed statistically significant differences between the control (unexposed) animals and the two groups of exposed animals by ANOVA weighted for unequal variance (heterogeneity of variances was found by Levene’s test), followed by Tukey’s post hoc test at the level of significance of p< 0.05. The two groups of lead-exposed animals were also significantly different from each other. Orally lead-exposed animals showed a significant increase of micronuclei frequencies in reticulocytes and erythrocytes compared to unexposed animals (ANOVA, p< 0.05).

Excitatory amino acids and lead-induced neurotoxicity

Abstract: The NMDA receptor non-competitive antagonist, [3H] MK-801, was used as a ligand for an autoradiographic study to determine the effects of lead on NMDA receptor in rat brain. Adult male rats were given lead acetate, 100 mg/kg, or sodium acetate, 36 mg/kg (control), by i. p. for 7 days. Lead levels were detected in blood (41.1μg/dl) and brain (16.7-29.4μg/g). Concentrations of lead in various brain regions did not differ. [3H] MK-801 binding was heterogeneous throughout the brain with the following order of binding densities : hippocampal formation>cortex>caudate-putamen>thalamus>brainstem. Lead exposure caused a decrease in [3H] MK-801 binding to NMDA receptors in the hippocampal formation including CA2 stratum radiatum, CA3 stratum radiatum and presubiculum, and in the agranular insular, cingulate, entorhinal, orbital, parietal and perihinal areas of cerebral cortex. In another experiment, female rates were exposed pre-and post-natally from the 4th±1 post cconception day with 1, 000 ppm lead in their drinking water. This treatment continued after weaning. No effects of lead on [3H] MK-801 binding were found at postnatal day (PM) 28. However, lead caused a significant increase in [3H] MK-801 binding in the hippocampus including CA1 and CA2, and in the occipital and temporal cortical areas at PN 56 and at PN 112. Increases in [3H] MK-801 binding were also found in entorhinal cortex and dentate gyrus at PN 112. The hippocampal formation is a critical neural structure for learning and memory processes, whereas cortical and subcortical regions are involved in the modulation of complex behavioral processes. NMDA receptors have been shown to play a key role in synaptic plasticity underlying learning and memory. Therefore, lead-induced alterations of ligand binding to NMDA receptors in the hippocampal formation and cortical areas may play a role in lead-induced neurotoxicity.

Protective effect of some antioxidants on the brain of adult male albino rats, Rattus rattus, exposed to heavy metals.

Abstract: Adult male albino rats were exposed to 100 mg/L of lead acetate or 100 mg/L sodium arsenate in drinking water for 3 and 6 weeks, lead and arsenic inhibit cholinesterase activity after both time intervals, with percentage reached 23% and 25% in lead and arsenic after 6 weeks, respectively. The results revealed that lead or arsenic leading to increase in relative brain weight in most of the experimental period. Using antox, (an antioxidant contains three supplementary nutritional vitamins A, C and E with rare element selenium) with lead or arsenic led to an improvement of serum cholinesterase activity in rats and also relative brain weight. Histological studies showed that lead and arsenic treated rats induced neuron injuries and change in brain cells. Rats treated with antox during administration of lead or arsenic repair some injuries of brain cells and neuron induced by lead or arsenic. Rats treated with both lead or arsenic and antox revealed an improvement in histopathological alteration induced by lead or by arsenic after 3 weeks and 6 weeks. This proved the effectiveness of antox that attributed to its antioxidant properties. In conclusion, heavy metals i.e. lead and arsenic proved severely neurotoxic and antox reduces the resulting damage probably due to its ability to neutralize free radicals that are generated by lead and arsenic.

Effects of Maternal Lead Acetate Exposure during Lactation on Postnatal Development of Testis in Offspring Wistar Rats

Abstract: Objective(s) During recent years, there has been an increasing interest in contribution of environmental pollutants as heavy metals to human male infertility. Present study was aimed to investigate the effects of maternal lead acetate exposure during lactation on postnatal development of testis in offspring rats. Materials and Methods A total of 60 female rats randomly divided into four equal groups; control and three treatment groups received 20, 100 and 300 mg/kg/day lead acetate via drinking water from day 2 to day 21 of lactation. At 7, 14, 21, 28, 60, 90 and 120 days after birth, the testis weight and volume of offspring were measured and their epididymal semen analyzed. Following tissue processing, 5 µm sections were stained with haematoxylineosin and evaluated with quantitative techniques. Testicular parameters in different groups were compared by one-way ANOVA. Results Testis weight and volume of offspring decreased significantly in a dose-related manner in moderate (P< 0.05) and high (P< 0.01) doses groups. Dose-dependent significant reductions were seen in seminiferous tubules diameter and germinal epithelium height during neonatal, prepubertal and postpubertal periods in moderate (P< 0.05) and high (P< 0.01) doses groups until 90 and 120 days after birth, respectively. Significant decreases were observed in mean sperm density of offspring at puberty in moderate and high doses groups until 90 and 120 days after birth, respectively. Testosterone levels decreased significantly in a dose-related manner at puberty in moderate and high doses groups. Conclusion