Behavioral effects of moderate lead exposure in children and animal models: Part 2, animal studies

Bornschein, Robert L.; Pearson, Douglas T.; Reiter, Lawrence W.; Grant, Lester D.

doi:10.3109/10408448009037492

Cited by 41 publications

(10 citation statements)

References 72 publications

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“…Animal studies predicted a role for the b-adrenoceptors of brain in memory (Severson 1984). The studies on the behavioral toxicity of inorganic lead in animals have been reviewed by Bornschein et al (1980), Jason and Kellog (1980), Michaelson (1980), and Winneke (1986).…”

Section: Groupmentioning

confidence: 98%

?-adrenergic receptor density and adenylate cyclase activity in lead-exposed rat brain after cessation of lead exposure

Chang

Tsao

et al. 2004

Arch Toxicol

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To understanding the reversible or irreversible harm to the beta-adrenergic system in the brain of lead-exposed rats, this study sets up an animal model to estimate the change in the sympathetic nervous system of brain after lead exposure was withdrawn. We address the following topics in this study: (a) the relationship between withdrawal time of lead exposure and brain beta-adrenergic receptor, blood lead level, and brain lead level in lead-exposed rats after lead exposure was stopped; and (b) the relationship between lead level and beta-adrenergic receptor and cyclic AMP (c-AMP) in brain. Wistar rats were chronically fed with 2% lead acetate and water for 2 months. Radioligand binding was assayed by a method that fulfilled strict criteria of beta-adrenergic receptor using the ligand [125I]iodocyanopindolol. The levels of lead were determined by electrothermal atomic absorption spectrometry. The c-AMP level was determined by radioimmunoassay. The results showed a close relationship between decreasing lead levels and increasing numbers of brain beta-adrenergic receptors and brain adenylate cyclase activity after lead exposure was withdrawn. The effect of lead exposure on the beta-adrenergic system of the brain is a partly reversible condition.

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Section: Groupmentioning

confidence: 98%

?-adrenergic receptor density and adenylate cyclase activity in lead-exposed rat brain after cessation of lead exposure

Chang

Tsao

et al. 2004

Arch Toxicol

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“…Bressler and Goldstein, 1991). Exposure to lead was shown to produce neurobehavioral deficits such as ataxia (Bornschein et al, 1980), and, in the long run, hyperactivity, increased rearing and grooming, and decreased exploratory behavior (Goyer, 1993;Ma et al, 1999;Moreira et al, 2001;Trombini et al, 2001). The present study was conducted to assess the effect of lead exposure on motor activity, as measured by horizontal locomotion in an open field, using adult mice from several strains.…”

Section: Introductionmentioning

confidence: 99%

“…Lead is thought to be involved in many neurophysiological and behavioral pathologies in humans and laboratory animals (Bornschein et al, 1980). The magnitude of these effects depends on several factors, including the type and intensity of exposure, and the age of the subjects.…”

Section: Introductionmentioning

confidence: 99%

Motor behavior and brain enzymatic changes after acute lead intoxication on different strains of mice

2004

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“…Understanding of the associated mechanistic effects of lead and zinc on learning and memory alterations in central nervous system (CNS) is very important to be investigated [2][3][4][5]. From such experimental studies, exposure to lead (Pb) can cause serious neurotoxic effects at the molecular [6], cellular [7], and behavioral levels [8,9]. On the other hand, there are reports about the memory impairments, apoptosis, and cytotoxicity induced by excess levels of zinc consumption [10].…”

Section: Introductionmentioning

confidence: 99%

Zinc Chloride and Lead Acetate-Induced Passive Avoidance Memory Retention Deficits Reversed by Nicotine and Bucladesine in Mice

Tabrizian

Yazdani

Baheri

et al. 2015

Biol Trace Elem Res

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It is very important to investigate the neurotoxic effects of metals on learning and memory processes. In this study, we tried to investigate the effects and time course properties of oral administration of zinc chloride (25, 50, and 75 mg/kg, for 2 weeks), lead acetate (250, 750, 1,500, and 2,500 ppm for 4, 6 and 8 weeks), and their possible mechanisms on a model of memory function. For this matter, we examined the intra-peritoneal injections of nicotine (0.25, 0.5, 1, and 1.5 mg/kg) and bucladesine (50, 100, 300, and 600 nM/mouse) for 4 days alone and in combination with mentioned metals in the step-through passive avoidance task. Control animals received saline, drinking water, saline, and DMSO (dimethyl sulfoxide)/deionized water (1:9), respectively. At the end of each part of studies, animals were trained for 1 day in step-through task. The avoidance memory retention alterations were evaluated 24 and 48 h later in singular and combinational studies. Zinc chloride (75 mg/kg) oral gavage for 2 weeks decreased latency times compared to control animals. Also, lead acetate (750 ppm oral administrations for 8 weeks) caused significant lead blood levels and induced avoidance memory retention impairments. Four-days intra-peritoneal injection of nicotine (1 mg/kg) increased latency time compared to control animals. Finally, findings of this research showed that treatment with intra-peritoneal injections of nicotine (1 mg/kg) and/or bucladesine (600 nM/mouse) reversed zinc chloride- and lead acetate-induced avoidance memory retention impairments. Taken together, these results showed the probable role of cholinergic system and protein kinase A pathways in zinc chloride- and lead acetate-induced avoidance memory alterations.

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Behavioral effects of moderate lead exposure in children and animal models: Part 2, animal studies

Cited by 41 publications

References 72 publications

?-adrenergic receptor density and adenylate cyclase activity in lead-exposed rat brain after cessation of lead exposure

?-adrenergic receptor density and adenylate cyclase activity in lead-exposed rat brain after cessation of lead exposure

Motor behavior and brain enzymatic changes after acute lead intoxication on different strains of mice

Zinc Chloride and Lead Acetate-Induced Passive Avoidance Memory Retention Deficits Reversed by Nicotine and Bucladesine in Mice

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