Effects of postnatally administered inorganic lead on the tyrosine hydroxylase immunoreactive norepinephrinergic neurons of the locus ceruleus of the rat.
The neurotoxic effects of inorganic lead are known to include peripheral neuropathy in adults and encephalopathy in children. The purpose of this study was to determine the effect of inorganic lead (PbCl2) administration on norepinephrinergic neurons of the locus ceruleus in neonatal rats by immunocytochemical and electron microscopic analyses. Lead chloride solutions, 0.05%, 0.1% and 0.2% in concentrations, were prepared in distilled water and administered orally via drinking water. After 4, 8, or 12 weeks of continuous administration, the rats were sacrificed and brains were immunostained with the tyrosine hydroxylase antibody. The number of immunoreactive cell bodies in the locus ceruleus was estimated. Densitometric analysis of immunoreactive profiles visualized by electron microscopy was performed using an image analyzer. The numbers of immunoreactive neurons in the locus ceruleus were increased statistically by lead administration. The intensity of the immunoreaction, both under the light and electron microscopes was also increased. Degenerative changes, including intra-axonal vacuole formation and widening of the extracellular spaces, were found by electron microscopy in and around the tyrosine hydroxylase immunoreactive axons. Increased tyrosine hydroxylase immunoreactivity may correlate with the hyper-reactivity of lead intoxicated children. Degenerative changes may account for the reported deficits in intellectual attainment and achievement in lead intoxicated children. (+info)
Lead is one of the oldest known and most widely studied occupational and environmental toxins. Despite intensive study, there is still vigorous debate about the toxic effects of lead, both from low-level exposure in the general population owing to environmental pollution and historic use of lead in paint and plumbing and from exposure in the occupational setting. The majority of industries historically associated with high lead exposure have made dramatic advances in their control of occupational exposure. However, cases of unacceptably high exposure and even of frank lead poisoning are still seen, predominantly in the demolition and tank cleaning industries. Nevertheless, in most industries blood lead levels have declined below levels at which signs or symptoms are seen and the current focus of attention is on the subclinical effects of exposure. The significance of some of these effects for the overt health of the workers is often the subject of debate. Inevitably there is pressure to reduce lead exposure in the general population and in working environments, but any legislation must be based on a genuine scientific evaluation of the available evidence. (+info)
Protective effects of Hippophae rhamnoides L. juice on lead-induced neurotoxicity in mice.
We examined the effect of Hippophae rhamnoides L. (HRL) juice on lead-induced memory impairment and neuronal damage in the brains of adult mice. Kunming mice were exposed to lead acetate 10 mg/kg body weight for 20 d. Twenty percent and 40% HRL prevented the lead-induced decrease in step-through latency. In the water maze test, the swimming time was lengthened in mice treated with lead acetate, but this time was decreased in mice that received 20% and 40% HRL. The malondialdehyde (MDA) levels were increased in lead-treated mice, which were reduced by 20% and 40% HRL in dose-dependent manner. The activities of acetylcholinesterase (AchE) and monoamine oxidase-A and -B were significantly increased in the lead-treated group, which were decreased by 40% HRL but not by 20% HRL. The levels of norepinephrine, serotonin, and 5-hydroxyindole acetic acid were decreased significantly in the lead-treated mice, and the decreases were antagonized by 40% HRL, except for than in dopamine, but 20% HRL had no effect on this change. These data suggest that the different doses of the HRL juice protect against the lead acetate-induced deficits in learning and memory and changes in neurobiochemical parameters. (+info)
Plumbism or lead intoxication mimicking an abdominal tumor.
The clinical presentation of lead intoxication may vary widely and in the absence of a high clinical index of suspicion, the diagnosis may be missed. The effects of lead on mitochondrial oxidative phosphorylation and its interaction with calcium-mediated processes explain the heterogenous presentation. In this case report, the diagnosis was finally made when bilateral wrist drop developed on top of abdominal cramps and anemia. Before, ascites raised the suspicion of a tumor. Therefore, each element of the triad of unexplained anemia, abdominal cramps, and bilateral wrist (or foot) drop should lead any physician to consider the diagnosis of lead intoxication. This case also illustrates the importance of a careful and meticulous social history in patient management. (+info)
Inflammation-like glial response in lead-exposed immature rat brain.
Numerous studies on lead (Pb) neurotoxicity have indicated this metal to be a dangerous toxin, particularly during developmental stages of higher organisms. Astrocytes are responsible for sequestration of this metal in brain tissue. Activation of astroglia may often lead to loss of the buffering function and contribute to pathological processes. This phenomenon is accompanied by death of neuronal cells and may be connected with inflammatory events arising from the production of a wide range of cytokines and chemokines. The effects of prolonged exposure to Pb upon glial activation are examined in immature rats to investigate this potential proinflammatory effect. When analyzed at the protein level, glial activation is observed after Pb exposure, as reflected by the increased level of glial fibrillary acidic protein and S-100beta proteins in all parts of the brain examined. These changes are associated with elevation of proinflammatory cytokines. Production of interleukin (IL)-1beta and tumor necrosis factor-alpha is observed in hippocampus, and production of IL-6 is seen in forebrain. The expression of fractalkine is observed in both hippocampus and forebrain but inconsiderably in the cerebellum. In parallel with cytokine expression, signs of synaptic damage in hippocampus are seen after Pb exposure, as indicated by decreased levels of the axonal markers synapsin I and synaptophysin. Obtained results indicate chronic glial activation with coexisting inflammatory and neurodegenerative features as a new mechanism of Pb neurotoxicity in immature rat brain. (+info)
The relation of low-level prenatal lead exposure to behavioral indicators of attention in Inuit infants in Arctic Quebec.
The aim of this study was to investigate the association between prenatal exposure to lead (Pb) and several aspects of behavioral function during infancy through examiner ratings and behavioral coding of video recordings. The sample consisted of 169 11-month-old Inuit infants from Arctic Quebec. Umbilical cord and maternal blood samples were used to document prenatal exposure to Pb. Average blood Pb levels were 4.6 mug/dL and 5.9 mug/dL in cord and maternal samples respectively. The Behavior Rating Scales (BRS) from the Bayley Scales of Infant Development (BSID-II) were used to assess behavior. Attention was assessed through the BRS and behavioral coding of video recordings taken during the administration of the BSID-II. Whereas the examiner ratings of behaviors detected very few associations with prenatal Pb exposure, cord blood Pb concentrations were significantly related to the direct observational measures of infant attention, after adjustment for confounding variables. These data provide evidence that increasing the specificity and the precision of the behavioral assessment has considerable potential for improving our ability to detect low-to-moderate associations between neurotoxicants, such Pb and infant behavior. (+info)
Developmental lead exposure attenuates methamphetamine dose-effect self-administration performance and progressive ratio responding in the male rat.
Lead encephalopathy due to traditional medicines.
Traditional medicine use is common in developing countries and increasingly popular in the western world. Despite the popularity of traditional medicines, scientific research on safety and efficacy is limited. However documented fatalities and severe illness due to lead poisoning are increasingly recognized to be associated with traditional medicine use. As society becomes more globalized, it is imperative for pharmacists and health care providers to learn about the safety of traditional medical practices. The information presented educates and alerts pharmacists and health care providers about the potential of traditional medicines to cause lead encephalopathy. Case reports were located through systematic literature searches using MEDLINE, CINAHL, AMED, CISCOM, EMBASE and The Cochrane library from 1966 to the February 2007. Reference lists of identified articles and the authors' own files were also searched. Inclusion criteria were cases of human lead encephalopathy associated with traditional medical practices. There were no restrictions regarding the language of publication. Data were subsequently extracted and summarized in narrative and tabular form. We found 76 cases of lead encephalopathy potentially associated with traditional medicine. Ayurvedic medicines were associated with 5 cases (7%), Middle eastern traditional medicines with 66 cases (87%) and 5 cases (7%) with other traditional medicines. Of the 76 cases, 5% were in adults and 95% were in infants and young children. Of the 4 adult cases, at least one was left with residual neurological impairment. In infants and young children, among 72 cases 8 (11%) were fatal, and at least 15 (21%) had residual neurological deficits. Traditional medicine users should be screened for lead exposure and strongly encouraged to discontinue metal-containing remedies. Therefore, the United States Food and Drug Administration and corresponding agencies in other countries should require and enforce heavy metal testing for all imported traditional medicines and "dietary supplements". (+info)