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<b>Background and Objective:</b> Lead poisoning (Pb) is a big problem because it is found in almost all objects in daily life such as vehicle fuel, water pipes, ceramics, cosmetics and others. Continuous lead exposure can increase ROS resulting in an increase in hepatic IL-6 and caspase 3 which replaces hepatic cell apoptosis. The objective of this study was to determine the effect of <i>Apium graveolens</i> (celery) extract on plasma IL-6 and hepatic caspase 3 levels. <b>Materials and Methods:</b> This study used a post-test control group design. The research subjects were 20 Wistar rats that met the inclusion criteria and were divided into 4 groups randomly, namely (a) Sham group that had no treatment, (b) Negative control group was induced with lead acetate 200 mg kg¹ body weight/day without any treatment (c) Positive control group and (d) Treated group. On the 15th day, blood was taken to check IL-6 levels and tissue was taken for liver caspase 3 examination by immunohistochemical method. Data analysis used the one-way ANOVA test and continued with the <i>post hoc</i> LSD test. <b>Results:</b> The highest mean caspase 3 expression was in the control group 45.84±4.39 pg mL¹, while the mean of IL-6 plasma level was highest in the P1 641.33±39.72 pg mL¹ group. The Mann-Whitney test showed a significant difference in IL-6 levels between the study groups (p = 0.000). The Mann-Whitney test showed a significant difference in caspase 3 levels between the study groups (p = 0.000). <b>Conclusion:</b> Giving celery extract 300 mg kg¹ body weight/day affects plasma IL-6 and hepatic caspase 3 levels in lead acetate-induced rats.

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BACKGROUND: Although conventional electrophysiological parameters have been proposed as clinical indicators for monitoring lead neuropathies, their correlations with blood lead level are weak. In this study, we investigated the applicability of nerve excitability tests (NETs) to evaluate lead intoxication. METHODS: Fourteen workers who were exposed to lead with an elevated blood level ranging from 17.8 to 64.9 µg/dL and 20 healthy controls with similar ages and body heights were enrolled. Both workers and controls underwent nerve conduction studies (NCSs), motor evoked potentials (MEPs) with transcranial magnetic stimulation (TMS), and NETs. RESULTS: NCSs showed prolonged distal latencies and decreased motor nerve conduction velocity of median nerves in the workers but without significant correlation to blood lead level (BLL). Significantly prolonged MEP latency was observed in the workers (+ 6 ms). NETs demonstrated hyperpolarized resting membrane potentials in stimulus-response curves and changes in the property of potassium channels under a hyperpolarized current in threshold electrotonus, implying that lead hyperpolarized nerves by interfering with potassium channels. NETs also showed a better correlation with BLL than conventional electrophysiological parameters. CONCLUSIONS: Axonal hyperpolarization and central conduction delay are more apparently reflecting elevated BLL than NCS. NET may have the potential for early detection of lead neuropathy.

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Although many avian studies have investigated the toxic effects of lead on important biochemical and physiological processes, organ and system function, and behavior, studies evaluating the specific genotoxic effects of exposure to lead are scarce. Nowadays, rapid technological advances can provide new molecular techniques in this regard. In this study, as a novel approach in bird studies, we used a panel of ten microsatellite loci to investigate the microsatellite instability (MSI) in response to experimental lead intoxication in a common hole-nesting species, the great tit Parus major. For this purpose, an experiment based on an intentional single supplementation of a lead (II) acetate trihydrate compound was conducted, with the use of two different doses, applied to randomly chosen great tit nestlings from randomly selected broods, being at the stage of intensive erythropoiesis. Although this preliminary study did not find any MSI in the seven microsatellite markers retained for the final comparison, it contributes to the examination of this molecular technique in field conditions as being potentially applicable in ecotoxicological bird studies. We believe that certain issues should be considered in finding an explanation for our result. First, the single doses of lead used in this study may have been too weak to induce genetic instability. Second, the panel of microsatellite markers studied may have been unsusceptible to lead genotoxicity in general. Third, the relatively short time interval (5 days) between the experimental procedure (lead exposure) and the sampling of post-exposure material (blood) for genetic analyses could have limited the effect of lead genotoxicity. Further analyzes are needed to verify these findings and to evaluate the scope of application of the MSI analysis in wild bird population studies.

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Lead (Pb) intoxication is known to damage the proximal tubules of kidney. Autophagy and apoptosis have been shown to be involved in a variety of renal injuries, but the underlying mechanisms remain largely unknown. In this study, we constructed a mice model of Pb intoxication and validated it against lead concentrations in blood and urine. Electron microscopy revealed that Pb promoted the accumulation of autophagosomes. Subsequent immunofluorescence and western blotting revealed that Pb intoxication suppressed the autophagic flux. Next, exosomes were isolated and extracted through ultracentrifugation, and were further identified by diameter analysis and marker detection. We also demonstrated that autophagy and apoptosis were enhanced in renal cells with exosomes of Pb expose. Furthermore, the specific mechanisms were explored by RNA sequencing and it was found that several targeted genes regulated by differential exosomal miRNAs and lncRNAs. Target genes accumulated in several signaling pathways, especially the adenosine 5'-monophosphate-activated protein kinase (AMPK) signaling. We found that Pb intoxication-induced exosomes activated the AMPK signaling in renal proximal tubule cells. Furthermore, autophagy and apoptosis assays showed that GSK-690693, an AMPK inhibitor, significantly alleviated exosome-induced renal injuries by Pb intoxication. In conclusion, Pb-mediated exosome-induced autophagy and apoptosis via activating the AMPK signaling contributing to Pb-induced nephrotoxicity in renal cells.

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Fifteen hundred 12−15-month-old tropically adapted heifers inadvertently grazed a paddock which had a refuse dump in it containing burnt out vehicle batteries. The cattle grazed this paddock for approximately seven days. Subsequently these cattle were managed as two cohorts (cull and potential replacement breeding animals). Deaths commenced in the cull heifer group approximately 18 days after initial exposure to the refuse dump during relocation to a feedlot. Mortalities continued for 12 days, with other heifers showing clinical signs of marked central nervous system dysfunction requiring euthanasia. Necropsy of several clinically affected cattle plus blood sampling for lead analysis confirmed a diagnosis of lead intoxication. The crude mortality rate in the cull heifers was 6.6% (n = 685). Following confirmation of the diagnosis most of the potential replacement heifers (second cohort) were also relocated to the feedlot. The estimated crude mortality rate in this cohort was 5.8% (n = 815). All possible lead intoxication deaths occurred within 34 days of initial exposure, and apparently after day 16 at the feedlot no further heifers showed any clinical signs which could be attributed to lead intoxication. Longitudinal monitoring of blood lead concentrations was used to identify cattle suitable for slaughter. Overall, 70% of heifers initially blood sampled (n = 1408) had no detectable lead in their blood, however 16% had markedly elevated blood lead concentrations (> 0.7µmol/L) which persisted, and 2% had above the maximum normal threshold 1.5 years later. These latter cattle were subsequently euthanized, and necropsy revealed that visible pieces of lead were still present in the reticulum of several animals. At no time did any of these heifers with persistently high blood lead concentrations show clinical signs of lead intoxication.

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OBJECTIVE: The aim of the study was to study the effect of low and high doses of lead acetate on biochemical parameters and morphological status of rat ovaries in the experiment. PATIENTS AND METHODS: Materials and methods: The study was performed on 36 nonlinear female rats weighing 180-210 g, aged 4 months, divided into 3 experimental groups: I - control (C), II - rats, which were given 30 days to drink a solution of lead acetate with at the rate of 0,05 mg / kg of animal weight, group III - rats, which were given for 30 days to drink a solution of lead acetate at the rate of 60 mg/kg of animal weight. Biochemical research methods were included determination of diene conjugate concentration in animals' blood, concentration of TBA-active products, study of oxidative modification of proteins in blood plasma, determination of superoxide dismutase and catalase activities. Endogenous intoxication was assessed by the definition of medium-mass molecules, the content was expressed in units of extinction. The material for light microscopy investigation from the ovary was performed according to the generally accepted method. RESULTS: Results: Lead acetate causes activation of peroxidation of lipids and proteins in the body of female rats, which is directly dependent on the dose of lead. In response to the activation of free radical oxidation there are changes in the antioxidant system, which depend on the dose of lead acetate: at a dose of 0.05 mg / kg superoxide dismutase and catalase activity increase, at a dose of 60 mg / kg superoxide dismutase and catalase activity. Small doses of lead do not cause endogenous intoxication. Lead acetate causes the development of endogenous intoxication in animals only in large doses: increases the formation of toxic compounds, cell apoptosis, decreased excretory function of the kidneys, which is associated with multiorgan disorders. As a result of the action of lead acetate, morphological changes of the ovaries were observed, which increased with increasing dose of lead acetate. There was a dose-dependent decrease in massometric parameters, the number of follicles and changes in the thickness of the surface structures of the ovary, which is more pronounced at 60 mg/kg. CONCLUSION: Conclusions: Under the influence of small and large doses of lead acetate on biochemical changes in blood and morphological changes in the ovaries in male rats the oxidative stress is developed. Under the influence of small doses, the changes are adaptive, and under the influence of large doses - damaging.

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Lead (Pb) was revealed for its role as a neurodevelopmental toxin. The determination of neurotransmitters (NTs) in particular brain regions could ameliorate the precise description and optimization of therapeutic protocols able to restore the harmony of signaling pathways in nervous and immune systems. The determination of selected analytes from the group of NTs based on the liquid chromatography (LC)-based method was carried out to illustrate the changes of amino acid (AA) and biogenic amine (BA) profiles observed in chosen immune and nervous systems rat tissues after Pb intoxication. Also, a protective combination of AA was proposed to correct the changes caused by Pb intoxication. After the administration of Pb, changes were observed in all organs studied and were characterized by a fluctuation of NT concentrations in immune and nervous systems (hypothalamus samples). Using a protective mixture of bioactive compounds prevented numerous changes in the balance of NT. The combined analysis of the immune and nervous system while the normalizing effect of curative agents on the level of differentially secreted NTs and AA is studied could present a new approach to the harmonization of those two essential systems after Pb intoxication.

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Two different strands of hair taken from Beethoven's head after his death were examined for heavy metals using scanning electron microscopy (SEM) and laser ablation-ICP-MS (inductively coupled plasma-mass spectroscopy). The results revealed the presence of small lead particles on the surface of Beethoven's hairs and fluctuating lead levels in hair medulla along the length of the hair due to alternating lead exposure, with an average lead exposure of 100 times the normal value. The time-line attached to the peaks of these fluctuating values correlate with the pneumonia treatment and the paracenteses performed, including the subsequent treatment of the procedure wounds. While the administration of lead-containing drugs and treatments had been proven to resolve the pneumonia, it had simultaneously caused massive liver failure, accelerated by pre-existing cirrhosis. The question as to whether Beethoven's death was a case of malpractice can only be answered from a forensic point of view ex ante, since the state of the medical knowledge of the time has to be taken into account.

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BACKGROUND: Lead exposure is one of the most concerning public health problems worldwide, particularly among children. Yet the impact of chronic lead exposure on the thyroid status and related intelligence quotient performance among school-age children remained elusive. OBJECTIVE: The aim of this study was to evaluate the influence of lead exposure on the thyroid hormones, amino acid neurotransmitters balances, and intelligence quotient (IQ) among school-age children living nearby a lead-zinc mining site. Other factors such as rice lead levels, mothers' smoking behavior, and diet intake were also investigated. METHODS: A total of 255 children aged 7-12 years old were recruited in this study. Blood lead level (BLL), thyroid hormones including free triiodothyronine (FT3), free thyroxine (FT4) and thyroid stimulating hormone (TSH), and amino acid neurotransmitters such as glutamate (Glu), glutamine (Gln), and γ-aminobutyric acid (GABA) were measured using graphite furnace atomic absorption spectroscopy (GFAAS), chemiluminescence immunoassay, high performance liquid chromatography (HPLC). Raven's standard progressive matrices (SPM) and the questionnaire were used to determine IQ and collect related influence factors. RESULTS: The average BLL of children was 84.8 µg/L. The occurrence of lead intoxication (defined as the BLL ≥ 100 µg/L) was 31.8%. Serum TSH levels and IQ of lead-intoxicated children were significantly lower than those without lead toxicity. The GABA level of girls with the lead intoxication was higher than those with no lead-exposed group. Correlation analyses revealed that BLL were inversely associated with the serum TSH levels (R= -0.186, p < 0.05), but positively related with IQ grades (R = 0.147, p < 0.05). Moreover, BLL and Glu were inversely correlated with IQ. In addition, this study revealed four factors that may contribute to the incidence of lead intoxication among children, including the frequency of mother smoking (OR = 3.587, p < 0.05) and drinking un-boiled stagnant tap water (OR = 3.716, p < 0.05); eating fresh fruits and vegetables (OR = 0.323, p < 0.05) and soy products regularly (OR = 0.181, p < 0.05) may protect against lead intoxication. CONCLUSION: Lead exposure affects the serum TSH, GABA levels and IQ of school-aged children. Developing good living habits, improving environment, increasing the intake of high-quality protein and fresh vegetable and fruit may improve the condition of lead intoxication.

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Humic acids (HA) are natural substances which exhibit a remarkable spectrum of health benefits, such as their role in chelation. This study aims to supplement the current knowledge on the chelating effects of HA in chronic lead intoxication in rat femurs and in liver, heart and kidney mitochondria in an experiment lasting 10 weeks. Lead acetate trihydrate was administered to rats for 5 weeks at a daily dose of 155.5 mg/kg body weight. At the same time, rats were given three concentrations of HA, with their effect measured over the following 5 weeks. Increased Pb concentrations were detected in the femur after the first week, while HA-administered groups showed a tendency towards inhibiting the increase in Pb deposition. After 5 weeks, Pb concentrations dropped significantly in the HA groups. At the same time, however, other elements were redistributed, with a decrease in Se and Zn being particularly noteworthy. While an increase in Pb concentrations was found after 5 weeks of Pb administration, a concentration of 1% HA resulted in the least significant increase in Pb as well as an increase/decrease in Se/Cu, respectively. In mitochondria, an increase in Pb content was detected after the first and fifth weeks with concomitant redistribution of other elements. At the end of the experiment, again in the 1% HA group, Pb concentrations remained higher only in the liver with the other elements sufficiently normalized, indicating this concentration to be useful in the treatment of Pb intoxication.

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Lead (Pb) is recognized as one of the most toxic trace elements that can induce a wide range of negative health effects in wildlife. Because the investigation of basic environment-sensitive physiological indicators is easy to perform in wild birds, they have been considered as valuable bioindicators of lead contamination. The harmfulness of lead poisoning can depend on the type of exposure, and in most studies of birds, an effect of chronic lead exposition has been considered. In this study, we investigated whether a single exposure to specific doses of lead affected such physiological indices as haematocrit and the heterophil-to-lymphocyte ratio (H/L ratio). For this purpose, we conducted an experiment based on intentional lead supplementation, with the use of two different doses, applied to randomly chosen great tit (Parus major) nestlings from randomly selected broods. A few days after the exposure (when the nestlings were 15 days old), we determined haematocrit and the H/L ratio as potentially sensitive physiological indicators of lead intoxication. We found that the treatment with lead resulted in a significant decline in haematocrit level. In addition, we found that the age when lead exposure occurred can be considered as an important factor influencing haematocrit variation. A decrease in haematocrit was observed on consecutive days of nestling life. In contrast, the H/L ratio did not show any significant response to lead exposure. These results clearly show that the assessment of haematocrit level for nestling great tits can provide a simple and rapid method of indirect evaluation of physiological effects of lead intoxication caused by a single exposure.

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The increment of eryptosis in lead-exposed workers has been associated with oxidative stress, having as the main mediator [Ca2+]i. However, other molecules could participate as signals, such as PLA2 and SMase, which have been proposed to increase PGE2 and ceramides, both involved in the increment of PS externalization due to osmotic stress. To study the role of these enzymes in lead intoxication, we studied 30 lead exposed workers and 27 non-lead exposed individuals. We found, compared to non-exposed subjects, lead intoxication characterized by high blood lead concentration (median = 39.1 µg/dL), and low δ-ALAD activity (median = 348 nmol of porphobilinogen/h/mL); oxidative stress with high lipid peroxidation (median = 1.31 nmol of malondialdehyde/mL) and low TAC (median = 370 mM Trolox equivalents); a higher enzymatic activity of PLA2 (median = 518 AFU/mg) and SMase (median = 706 AFU/mg) and higher eryptosis (median = 0.92% PS externalization). Correlation and conditional probability analyses permit to associate oxidative stress and eryptosis with high PLA2 activity. However, high SMase activity was only associated with PLA2 activity. The role of these enzymes in the signal path to eryptosis induced by oxidative stress in lead-exposed workers is discussed.

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Chronic exposure to lead causes disruption to energy production mechanisms and tissue damage, in particular through its binding to thiol groups and competition for zinc binding sites. We investigated the possibility of preventing the consequences of chronic lead poisoning by administration of three different doses of humic acids (HAs) into feed with the aim of establishing an effective HA dose. During the 10-week experiment, a sub-lethal dose of lead acetate was given to rats during the first 5 weeks, with continuous administration of HA over 10 weeks. Measurements were taken to determine the content of the metals Pb, Mn, Cu, Fe and Zn; the metalloid Se; and selected antioxidant markers in the heart, liver, kidney and plasma after the first, fifth and tenth weeks of experiment. The administration of lead and HAs clearly affects the redistribution of the elements and the activity of the antioxidant enzymes. This fact was particularly highlighted in the lead-only group as, within the experiment, significantly higher Pb concentrations were found only in the plasma of this group. However, in the group with 1% HA administered with lead, we observed a rise in Zn concentrations in the organs and the deposition of Fe into the liver. Decreased glutathione reductase activity in the plasma and balanced reduced glutathione concentrations indicated sufficient efficiency of redox reactions. SOD activities were among those affected most strongly, with only the 1% HA group showing no effect on heavy metal redistribution as a result of HA administration.

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An adult, wild-caught electric eel ( Electrophorus electricus), weighing 18 kg and measuring 2 m in length, presented with bilateral swellings behind the pectoral fins, lethargy, and anorexia for 2 days. Anesthesia was performed with immersion in tricaine methanesulphonate and supplemented with 0.11 mg/kg medetomidine and 2.2 mg/kg ketamine intramuscularly. Endoscopy revealed blood in the oral and gastric cavity. The stomach was grossly enlarged, flaccid, and contained a lead wire which was removed manually. Blood lead values were severely elevated. The fish was treated with 28 mg/kg calcium disodium ethylenediaminetetraacetate intramuscularly every 72 hr for 5 doses, which resulted in an improved clinical condition. Because lead values had not decreased to normal values within 4 wk of initial presentation, 35 mg/kg dimercaptosuccinic acid was given orally twice weekly for 3 wk. The electric eel made a full recovery.

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Lead (Pb) pollution of aquatic habitats is a known threat to vertebrate health. Depending on Pb dosage, resulting symptoms can be chronic (sublethal) or acute (lethal). While acute exposure results in death of the animal, chronic sublethal exposure can also have consequences, reproduction, antioxidant defense and immunity being the most affected traits. While a great deal is known about Pb intoxication on avian health, relatively little is known about how intoxication impacts parasites dependent on their avian hosts. The effect of Pb on intestinal helminth species richness and infection intensity was investigated in mallards (Anas platyrhynchos, n = 100) from German waters. Coracoid bones were used to measure chronic Pb exposure. Intestinal helminths were characterized morphologically. Molecular approaches were also applied to identify poorly morphologically preserved parasites to obtain sequence data (cox1 gene) for species identification and future parasitological studies. Parasite species richness and infection intensity was found to be significantly lower in birds with higher chronic Pb levels suggesting both host and parasites respond to Pb exposure. Altered immune modulation in the avian host may be the underlying mechanisms of Pb triggered decrease of parasites. However, it also likely reflects differences in the susceptibility of different helminths to Pb. Cestode and acanthocephala species richness were particularly impacted by Pb exposure. We conclude that, Pb intoxication may both negatively impact avian host and parasite diversity in aquatic habitats.

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Outbred male rats were repeatedly injected IP with sub-lethal doses of lead acetate 3 times a week during 5 weeks. They developed an explicit, even if moderate, lead intoxication characterized by typical hematological and some other features. The next day after the last injection the heart of each animal was excised, and the trabecules and papillary muscles from the right ventricle were used for modeling in vitro isometric (with varying starting length of the preparation) regimes of the contraction-relaxation cycle with different preloads. Several well-established parameters of this model were found changed compared with the preparations taken from the hearts of healthy control rats. Background in vivo calcium treatment attenuated both systemic and cardiotoxic effects of lead to an extent. We show for the first time that subchronic intoxication with lead caused myocardial preparations in a wide range of lengths to respond by a decrease in the time and speed parameters of the isometric contraction while maintaining its amplitude and by a decrease in the passive stiffness of trabecules. The responses of the various heart structures are outlined, and the isomyosin ratio is shown to have shifted towards the slow isoform. Mechanistic and toxicological inferences from the results are discussed.

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Lead is an important heavy metal used worldwide in several applications, especially in industry. People exposed to lead can develop a wide range of symptoms associated with lead poisoning. Many effects of lead poisoning are reported in the literature, showing a compromising of whole body health, with symptoms related to cardiovascular, immune, bone, reproductive, hematological, renal, gastrointestinal, and nervous system. However, the molecular lead targets as well as the pathways affected by lead poisoning are not completely described. The aim of this study was to construct a map of metabolic pathways impaired in lead poisoning by evaluating which biomolecules are directly affected by lead. Through manual literature curation, we identified proteins which physically interact with lead and subsequently determined the metabolic pathways those proteins are involved with. At total, we identified 23 proteins involved with heme synthesis, calcium metabolism, neurotransmission, among other biological systems, which helps to understand the wide range of lead-poisoning symptoms.

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Both lead intoxication in early childhood and deficient bilirubin-binding capacity (BBC) of blood in jaundiced neonates indicate risk for brain damage. Zinc protoporphyrin (ZPP) is a biomarker for lead intoxication (PbI) as well as well as for iron deficiency. Under the leadership of Jack Aviv, Aviv Biomedical, Inc. developed robust hematofluorometers for point-of-care assays of ZPP in blood and for the high-affinity BBC of blood. These assays use just drops of whole blood and are simple, fast and inexpensive. ZPP by hematofluorometry has been used world-wide as a primary screen for lead intoxication since 1979. Recent clinical studies enabled by an Aviv Biomedical, Inc. bilirubin hematofluorometer have renewed interest in BBC-based assessment of neurotoxicity for improved management of neonatal jaundice. This article sketches Jack Aviv's contribution to the development and application of hematofluorometry.

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Herod the Great was appointed "king of Jews," to govern Judea, by the Roman Emperor and Senate. He lived from 73/74 BCE to 4 CE. He died with an illness and symptoms that have been the source of considerable speculation. Richard Strauss depicted Herod in his classic opera, "Salome." That opera was derived from a play of the same name by Oscar Wilde, which was based on an 1876 painting, "Salome Dancing Before Herod," by Gustave Moreau. The operatic Herod was afflicted with an illness characterized by dementia, hallucinations, paranoia, alcoholism (from drinking the Emperor's wine), violence, twitches, and sterility; different interpretations showed him also with falls, chills, shaking, thirst, forgetfulness, and sleepiness, for which we suggest the novel diagnosis of chronic lead intoxication (which can manifest to rheumatologists as saturnine gout). He had compatible symptoms (encephalopathy and neuromuscular abnormalities) and consumed excessive quantities of imperial wine, known to be highly contaminated with lead and likely associated with similar symptoms among Roman aristocracy. Herod's demented cruelties-an oppressive reign which including the beheading of John the Baptist-exacerbated the political climate and may have contributed to the subsequent violent 7-year revolt culminating in the destruction of the second temple. How different might history have been if Herod the Great had been abstemious?

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Lead exposure has been associated with several defective skeletal growth processes and bone mineral alterations. The aim of the present study is to make a more detailed description of the toxic effects of lead intoxication on bone intrinsic material properties as mineral composition, morphology and microstructural characteristics. For this purpose, Wistar rats were exposed (n=12) to 1000ppm lead acetate in drinking water for 90days while control group (n=8) were treated with sodium acetate. Femurs were examined using inductively coupled plasma optical emission spectrometry (ICP-OES), Attenuated Total Reflection Fourier transform infrared spectroscopy (ATR-FTIR), X-ray diffraction (XRD), and micro-Computed Tomography (µCT). Results showed that femur from the lead-exposed rats had higher carbonate content in bone mineral and (Ca2++Mg2++ Na+)/P ratio values, although no variations were observed in crystal maturity and crystallite size. From morphological analyses, lead exposure rats showed a decreased in trabecular bone surface and distribution while trabecular thickness and cortical area increased. These overall effects indicate a similar mechanism of bone maturation normally associated to age-related processes. These responses are correlated with the adverse actions induced by lead on the processes regulating bone turnover mechanism. This information may explain the osteoporosis diseases associated to lead intoxication as well as the risk of fracture observed in populations exposed to this toxicant.

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