Lead acetate

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

Early chronic lead exposure reduces exploratory activity in young C57BL/6J mice.

Abstract: Research has suggested that chronic low-level lead exposure diminishes neurocognitive function in children Tests that are sensitive to behavioral effects at lowest levels of lead exposure are needed for the development of animal models In this study we investigated the effects of chronic low-level lead exposure on exploratory activity (unbaited nose poke task), exploratory ambulation (open field task) and motor coordination (Rotarod task) in pre-adolescent mice C57BL/6J pups were exposed to 0 ppm (controls), 30 ppm (low-dose) or 230 ppm (high-dose) lead acetate via dams' drinking water administered from birth to postnatal day 28, to achieve a range of blood lead levels (BLLs) from not detectable to 1484 µg dl(-1) ) At postnatal day 28, mice completed behavioral testing and were killed (n = 61) BLLs were determined by inductively coupled plasma mass spectrometry The effects of lead exposure on behavior were tested using generalized linear mixed model analyses with BLL, sex and the interaction as fixed effects, and litter as the random effect BLL predicted decreased exploratory activity and no threshold of effect was apparent As BLL increased, nose pokes decreased The C57BL/6J mouse is a useful model for examining effects of early chronic low-level lead exposure on behavior In the C57BL/6J mouse, the unbaited nose poke task is sensitive to the effects of early chronic low-level lead exposure This is the first animal study to show behavioral effects in pre-adolescent lead-exposed mice with BLL below 5 µg dl(-1)

Alteration in plasma corticosterone levels following long term oral administration of lead produces depression like symptoms in rats

Abstract: Lead toxicity is known to induce a broad range of physiological, biochemical and behavioral dysfunctions that may result in adverse effects on several organs, including the central nervous system. Long-term exposure to low levels of lead (Pb2+) has been shown to produce behavioral deficits in rodents and humans by affecting hypothalamic-pituitary-adrenal (HPA) axis. These deficits are thought to be associated with altered brain monoamine neurotransmission and due to changes in glucocorticoids levels. This study was designed to investigate the effects of Pb2+exposure on growth rate, locomotor activity, anxiety, depression, plasma corticosterone and brain serotonin (5-HT) levels in rats. Rats were exposed to lead in drinking water (500 ppm; lead acetate) for 5 weeks. The assessment of depression was done using the forced swimming test (FST). Estimation of brain 5-HT was determined by high-performance liquid chromatography with electrochemical detection. Plasma corticosterone was determined by spectroflourimetric method. The present study showed that long term exposure to Pb2+ significantly decreased the food intake followed by the decrease in growth rate in Pb2+exposed rats as compared to control group. No significant changes in open field activity were observed following Pb2+exposure while significant increase in anxiogenic effect was observed. Increased plasma corticosterone and decreased 5-HT levels were exhibited by Pb2+exposed rats as compared to controls. A significant increase in depressive like symptoms was exhibited by Pb2+exposed rats as compared to control rats. The results are discussed in the context of Pb2+ inducing a stress-like response in rats leading to changes in plasma corticosterone and brain 5-HT levels via altering tryptophan pyrrolase activity.

Effects of zinc coadministration on lead toxicities in rats.

Abstract: In order to investigate the effects of Zn on Pb toxicities. Proportion of abnormal sperm, percentage of micronucleated polychromatic erythrocyte (MPCE), serum thyroid hormones (T3, T4) and cortisol were measured. Rats received intraperitoneal injection of 25 mg/kg Pb acetate, 4 mg/kg Zn acetate, both Pb acetate and Zn acetate, or normal saline as controls, once every two days, 7 times in total. No significant differences in whole blood Pb were detected between groups received Pb alone or both Pb and Zn. On the contrary, the concentration of whole blood Zn in the group given Zn alone was significantly higher than that in the group that received both Pb and Zn. In the groups given Pb alone or both Pb and Zn, proportion of abnormal sperm, frequency of MPCE and serum cortisol were significantly higher than those in controls, whereas serum T3 and T4 were significantly lower than in controls. In the group given both Pb and Zn, T4 was decreased most obviously among the four groups. While the proportion of abnormal sperm was less in the group given both Pb and Zn than in the group given Pb alone. These findings suggest that Zn coadministration might alleviate toxic effects of Pb on the male reproductive system, whereas it could enhance the toxicity on thyroid function. Zn did not affect the toxicities of Pb on cytogenetic systems as indicated by MPCE percentage, and on serum cortisol levels under the dose of the present study. Our results suggested the double-edged effects of Zn on Pb toxicities in different organs. Therefore, the effects of Zn on Pb toxicities should be evaluated systematically.