Effects Of Pb Exposure Research Articles

Lead (Pb) Exposure on Hemoglobin Levels and Decreasing Lung Function of Fuel Station Workers Banjarmasin

Introdution:Exposure to airborne pollutants such as lead (Pb) can cause health problems. Fuel stations are one of the places with a high risk of Pb exposure sourced from fuel or motor vehicle exhaust emissions. This research aims to know the effect of Pb exposure on hemoglobin levels and lung function in fuel station workers. Methods: This study was observational, analytical, and cross-sectional on 40 fuel station workers in South Banjarmasin District. Urinary Pb measurement was carried out by spectrophotometry, then the relationship to peripheral blood hemoglobin (Hb) levels and lung function was analyzed based on FEV1 (%), FVC (%), and FEV1/FVC ratio with a simple linear regression test. The data met the classical assumptions of normality, heteroscedasticity, and with no autocorrelation. If abnormal distribution was found, data transformation was carried out. Results: Study obtained urinary Pb levels below the normal threshold of 0.0356±0.0074 ppm. Respectively, urinary Pb levels did not have a significant effect on Hb levels (mean±SD:14.39±1.41, adjusted R2:6.2%, p=0.067), FEV1 (94.15±6.93, 5.8%, p=0.074) and FVC (89.68±6.24, 0.5%, p=0.380). However, urinary Pb significantly correlated with decreasing the FEV1/FVC ratio (90.87±3.36, 10%, p=0.026) with the equation y=96.550159.454x even without any obstruction value. Conclusion: This study showed that urinary Pb levels were normal. An increase in urinary Pb levels has a significant effect on decreasing the FEV1/FVC ratio. Prevention to reduce the health impacts of Pb needs to be taken. More research on at-risk populations with longer years of service needs to be done

Sex and tissue-specificity of piRNA regulation in adult mice following perinatal lead (Pb) exposure

ABSTRACT Lead (Pb) is a neurotoxicant with early life exposure linked to long-term health effects. Piwi-interacting RNAs (piRNAs) are small non-coding RNAs that associate with PIWIL proteins to induce DNA methylation. It remains unknown whether Pb exposure influences piRNA expression. This study evaluated how perinatal Pb exposure (32 ppm in drinking water) impacts piRNA expression in adult mice and assessed piRNA dysregulation as a potential mechanism for Pb-induced toxicity. Pb exposure effects on piRNA expression and associated gene repression in the germline (testis/ovary) and soma (liver and brain) were evaluated. Small RNA sequencing was used to determine differentially expressed piRNAs, RT-qPCR to examine piRNA target expression, and whole genome bisulfite sequencing to evaluate target DNA methylation status. Three piRNAs (mmpiR-1500602, mmpiR-0201406, and mmpiR-0200026) were significant after multiple testing correction (all downregulated in the male Pb-exposed brain in comparison to control; FDR < 0.05). Within piOxiDB, TAO Kinase 3 was identified as a downstream mRNA target for one of the three Pb-sensitive piRNA. The Pb-exposed male brain exhibited increased Taok3 expression (p < 0.05) and decreased DNA methylation (FDR < 0.01). The results demonstrate that perinatal Pb exposure stably influences longitudinal piRNA expression in a tissue- and sex-specific manner, potentially via DNA methylation-directed mechanisms.

Effect of Pb-exposure and B vitamin deficiencies on δ-aminolevulinic acid dehydratase activity among workers from Pb recycling plants.

Previous studies reported that Pb exposure causes a negative association with delta-aminolevulinic acid dehydratase activity (δ-ALAD), but the impact of Pb exposure (dose and time), B vitamin deficiencies, and lifestyle factors needs to be explored. In this study, the impact of Pb exposure, B vitamin deficiencies, and lifestyle factors on δ-ALAD activity among workers exposed to Pb from the Pb-recycling process was evaluated. Blood lead levels (BLLs), B vitamins (B6, B9, and B12), hematological factors (Hb% and HCT), lifestyle factors, and δ-ALAD activity was assessed in 170 male Pb-exposed workers engaged in the Pb recycling process. BLLs are estimated using the ICP-OES method. B vitamins in serum samples from workers were determined using the ELISA method. The δ-ALAD activity in whole blood samples was determined using the spectrophotometer method. The lifestyle factors were collected using a standard questionnaire. The δ-ALAD activity was significantly decreased in workers with the habits of alcohol use, tobacco consumption, hematocrit < 41%, mild and moderate categories of anemia, vitamin B6 and B12 deficiency, and BLL categories of 10-30, 30-50, and > 50µg/dL. Multiple regression analysis revealed that the independent variables of alcohol consumption (β = -0.170; P = 0.025), BLLs (β = -0.589; P = 0.001) and Hb% (β = 0.183; P = 0.001) significantly influenced the δ-ALAD activity with 44.2% (R2 = 0.442). Among the workers exposed to Pb from the Pb recycling plant, δ-ALAD activity was considerably reduced by Pb exposure, B vitamin deficiency, hematological parameters, and lifestyle factors.

The Exposure to Lead (Pb) Exacerbates Immunological Abnormalities in BTBR T+ Itpr3tf/J Mice through the Regulation of Signaling Pathways Relevant to T Cells.

Autism spectrum disorder (ASD) is a common neurodevelopmental illness characterized by abnormal social interactions, communication difficulties, and repetitive and limited behaviors or interests. The BTBR T+ Itpr3tf/J (BTBR) mice have been used extensively to research the ASD-like phenotype. Lead (Pb) is a hazardous chemical linked to organ damage in the human body. It is regarded as one of the most common metal exposure sources and has been connected to the development of neurological abnormalities. We used flow cytometry to investigate the molecular mechanism behind the effect of Pb exposure on subsets of CD4+ T cells in the spleen expressing IFN-γ, T-bet, STAT1, STAT4, IL-9, IRF4, IL-22, AhR, IL-10, and Foxp3. Furthermore, using RT-PCR, we studied the effect of Pb on the expression of numerous genes in brain tissue, including IFN-γ, T-bet, STAT1, STAT4, IL-9, IRF4, IL-22, AhR, IL-10, and Foxp3. Pb exposure increased the population of CD4+IFN-γ+, CD4+T-bet+, CD4+STAT1+, CD4+STAT4+, CD4+IL-9+, CD4+IRF4+, CD4+IL-22+, and CD4+AhR+ cells in BTBR mice. In contrast, CD4+IL-10+ and CD4+Foxp3+ cells were downregulated in the spleen cells of Pb-exposed BTBR mice compared to those treated with vehicle. Furthermore, Pb exposure led to a significant increase in IFN-γ, T-bet, STAT1, STAT4, IL-9, IRF4, IL-22, and AhR mRNA expression in BTBR mice. In contrast, IL-10 and Foxp3 mRNA expression was significantly lower in those treated with the vehicle. Our data suggest that Pb exposure exacerbates immunological dysfunctions associated with ASD. These data imply that Pb exposure may increase the risk of ASD.

Does Occupational Lead Exposure Affect the Relationship Between Neurobehavioral Characteristics and Productivity?

Background &amp; Aims: Lead (Pb) may cause cognitive impairments in both recent acute and chronic exposures. In this study, the effect of Pb exposure on the relationship between neurobehavioral characteristics and productivity was evaluated among battery manufacturing workers. Materials and Methods: In general, 179 production workers and 179 office workers participated in this cross-sectional study. Venous blood sampling was used to measure the level of Pb in the blood. Psychomotor performance and intellectual functioning were measured using the digit symbol substitution test and the Wechsler adult intelligence scale-revised, respectively. Finally, productivity was assessed using a health and work performance questionnaire. Results: Exposed workers had a significantly higher level of Pb, while a lower level of intellectual functioning and psychomotor performance than non-exposed workers. The results of linear regression indicated that the increase in the blood level of Pb was accompanied by a significant decrease in the positive effects of intellectual functioning on productivity. However, exposure to Pb had no effect on the relationship between psychomotor performance and productivity. Conclusion: Occupational exposure to Pb affected the relationship between psycho-diagnostic performance and productivity and could induce neurobehavioral dysfunction in the exposed workers. For the early detection of cognitive impairment, the neurobehavioral assessment is recommended to be implemented in work assessments.

Lead exposure induces structural damage, digestive stress, immune response and microbiota dysbiosis in the intestine of silver carp (Hypophthalmichthys molitrix)

Lead (Pb) is one of the most common trace metals in water, and its high concentration in the environment can cause harm to aquatic animals and humans. In the present study, the effects of Pb exposure (3.84 mg/kg) on the morphology, digestive enzyme activity, immune function and microbiota structure of silver carp (Hypophthalmichthys molitrix) intestines within 96 h were detected. Moreover, the correlation between them was analyzed. The results showed that Pb exposure on the one hand severely impaired the intestinal morphology, including significantly shortening the intestinal villi's length, increasing the goblet cells' number, causing the intestinal leukocyte infiltration, and thickening the intestinal wall abnormally, on the other hand, increasing the activity of intestinal digestive enzyme (trypsin and lipase). In addition, the mRNA expressions of structure-related genes (Claudin-7 and villin-1) were down-regulated, and the immune factors genes (IL-8, IL-10 and TNF-α) were up-regulated after Pb exposure. Furthermore, data of the MiSeq sequencing showed that the abundance of membrane transport, immune system function and digestive system of silver carp intestinal microbiota all decreased, while cellular antigens increased. Finally, the canonical correlation analysis (CCA) showed that there were correlations between silver carp's intestinal microbiota and intestinal morphology and immune factors. In conclusion, it is speculated that the entry of Pb into the intestine leads the microbiota dysbiosis, affects the intestinal immunity and digestive function, and further damages the intestinal barrier of silver carp.

SIRT1 modifies DNA methylation linked to synaptic deficits induced by Pb in vitro and in vivo

To investigate the mechanism of Silent information regulator 1 (SIRT1) regulation of DNA methylation and thus the expression of synaptic plasticity-related genes induced by lead (Pb) exposure, the early-life Sprague-Dawley rats and PC12 cells were used to establish Pb exposure models and treated with SIRT1 agonists (resveratrol and SRT1720). In vivo results demonstrated that Pb exposure increased the expression of DNMTs, MeCP2, PP1 and cleaved caspase3, decreased the expression of SIRT1, BDNF and RELIN and altered DNA methylation levels of synaptic plasticity genes. Moreover, we observed marked pathological damage in the hippocampal CA1 region of the 0.2 % Pb-exposure group. After treatment with resveratrol, the effects of Pb exposure on the expression of the above molecules and pathological features were significantly ameliorated in the hippocampus of rats. In vitro results showed that after the treatment with SRT1720, the expression of SIRT1 was activated and thus reversed the effect on DNMTs, MeCP2, apoptosis and synaptic plasticity-related genes and their DNA methylation levels induced by Pb exposure. In conclusion, we validated the important protective role of SIRT1 in neurotoxicity induced by Pb exposure through in vivo and in vitro experiments, providing potential therapeutic targets for the treatment and prevention of brain damage.

Urban heavy metal contamination limits bumblebee colony growth

Abstract Post‐industrial shrinking cities contain abundant vacant land and are increasingly recognized for their pollinator conservation potential. At the same time, the industrial legacies of these urban ecosystems have resulted in elevated levels of heavy metals in surface soils, which could negatively affect bee populations. We investigated whether foraging within heavy metal contaminated landscapes represents a fitness cost for the common Eastern bumblebee Bombus impatiens, by placing colonies in residential backyards along an urban to rural gradient extending south and east from the city of Cleveland, Ohio, USA. Bees foraged in the landscape for 3 weeks, after which time we counted the total number of workers and larvae present in the colony and analysed castes for the presence of heavy metals. We then assessed the relationship between landscape composition, heavy metal loads and caste abundance. Colonies located in urban landscapes were more likely to be exposed to lead (Pb). Elevated concentrations of Pb within workers were negatively correlated with both the number of workers and the number of larvae present. Synthesis and applications. Our findings raise concern that lead (Pb) contamination could represent a significant challenge to bee conservation in cities. To elucidate risks posed by this pollutant, we highlight a need to quantify lethal and sub‐lethal effects of Pb exposure using laboratory and field‐based studies. Further, identifying routes of exposure and landscape factors that influence exposure risk is necessary to implement mitigation strategies as part of urban conservation initiatives.

Lead exposure and its interactions with oxidative stress polymorphisms on lung function impairment: Results from a longitudinal population-based study

Exposure to lead (Pb) and cadmium (Cd) were related to lung function impairment, and this association may be modified by genetic variants in oxidative stress response. Here we enrolled 1243 coke-oven workers in a prospective cohort who were followed up from 2010 to 2014, assessed the associations of Pb and Cd exposure with 4-year lung function impairment, and further explored the interaction effects of Pb with 2664 single nucleotide polymorphisms (SNPs) in 345 oxidative stress related genes. Urinary levels of Pb, Cd, and two oxidative stress biomarkers [8-iso-prostaglandin F2α (8-iso-PGF2α) for lipid peroxidation and 8-hydroxy-2′-deoxyguanosine (8-OHdG) for oxidative DNA damage] were measured at baseline only and their lung function levels were measured both at baseline and at the end of follow-up. Each 10-fold increase in urinary Pb was associated with −159 (95%CI: −254, −64.2) mL and −3.63% (95%CI: −6.48%, −0.78%) changes in FEV1 and percent predicted FEV1 (ppFEV1), respectively. But none significant associations were observed for Cd. NQO1 rs2917670 showed significant interaction with Pb on elevated FEV1 decline after multiple comparison (Pint=1.54 × 10−5). In addition, urinary Pb increased with 8-iso-PGF2α and the rs2917670-C could significantly decrease NQO1 expression in normal lung tissues. These findings suggested the gene-environmental interaction of NQO1 rs2917670 and Pb exposure on the reduction of FEV1. The effect of Pb exposure on elevated oxidative stress and the decreased expression of antioxidant enzyme NQO1 caused by rs2917670-C allele may partly explain the underlying biological mechanism.

Low dose lead exposure at the onset of puberty disrupts spermatogenesis-related gene expression and causes abnormal spermatogenesis in mouse

Implications of lead (Pb) exposure in dysregulated spermatogenesis in sexually active individuals during adulthood is well established; however, the effect of Pb exposure on spermatogenesis in the early stages of puberty is not clear yet. Moreover, the mechanism of Pb mediated dysregulation of spermatogenesis in adults is also poorly understood. Exposure to environmental toxicants during puberty may cause serious consequences in adulthood causing developmental retardations, especially in the reproductive system. Here we investigated the effects of lead exposure on spermatogenesis at the onset of puberty and the underlying mechanisms of these effects. Male ICR mice were exposed to low (50 mg/L) and high (200 mg/L) doses of Pb through the drinking water for 90 days. At the end of this period, the blood Pb level of the low-dose and high-dose exposure groups were found 6.14 ± 0.34 μg/dL and 11.92 ± 2.92 μg/dL respectively which were in agreement with the US CDC-recommended (5 μg/dL) and Chinese CDC-recommended (10 μg/dL) reference blood Pb level for the children. Although no visible toxicity was observed in either group, Pb exposure caused considerable histopathological changes in testis and epididymis; increased sperm DNA fragmentation indices as well as disrupted sperm heads and head-neck conjunctions. Moreover, both low and high-dose Pb exposures caused aberrant expressions of several important spermatogenesis-related genes in epididymis and testis. These results suggest that although the blood Pb levels are close to the recommended-reference values, low dose Pb exposure at the onset of puberty can disrupt spermatogenesis-related gene expression and cause abnormal mouse spermatogenesis.

Lead accumulation and soil microbial activity in the rhizosphere of the mining and non-mining ecotypes of Athyrium wardii (Hook.) Makino in adaptation to lead-contaminated soils.

Better understanding of microbial activity in the rhizosphere soils associated with lead (Pb) uptake by plants may help with the phytoremediation of Pb-contaminated soils. In this work, the effects of Pb exposure (0, 200, 400, 600, 800 mg kg-1) on Pb accumulation and soil microbial activity in the rhizosphere of the mining ecotype (ME) and corresponding non-mining ecotype (NME) of Athyrium wardii (Hook.) Makino were investigated through a pot experiment. Although the plant growth of the two ecotypes was inhibited under Pb stress, the ME showed a less biomass decrease (12.6-44.0%) for aboveground than the NME, showing a greater tolerance to Pb stress. Pb concentrations as well as Pb accumulation in the two ecotypes showed an increasing trend with increasing soil Pb concentrations. The ME presented greater Pb accumulation ability than the NME, especially in underground parts. Pb availability in the rhizosphere soils of the two ecotypes after harvest decreased compared with those before transplantation. Available Pb in the rhizosphere of the ME was 1.4-4.8 times higher than that of the NME under exposure to 200-800 mg kg-1 Pb. The ME shows a greater ability to mobilize Pb in the rhizosphere soils. Pb exposure resulted in an inhibition of microbial activity in the rhizosphere of the two ecotypes. The ME demonstrated greater soil respiration and microbial biomass carbon (MBC) in the rhizosphere than the NME when treated with 200-800 mg kg-1 Pb. The ME showed a less decrease for MBC and a less increase for metabolic quotient in the rhizosphere soils than the NME when exposed to Pb generally. Microorganisms in the rhizosphere soils of the ME seem to be much more adapted to Pb stress, thus showing a great benefit for Pb accumulation and the phytostabilization of Pb-contaminated soils by the ME.

Assessment of Serum Magnesium Fractions in Workers Exposed to Pb from Pb-Battery Plant.

Most of studies assessed the effect of Pb-exposure on serum total magnesium (tMg). The hypomagnesium condition depended on protein concentration in the sample and influence of lifestyle factors. This study assessed the effect of Pb- exposure on serum tMg, corrected Mg (cMg), ionized Mg (iMg), percentage of iMg from tMg, and percentage of iMg from cMg with contemplation of lifestyle factors. Case control study. The serum magnesium fractions were assessed in 176 male Pb-exposed workers in the year 2015 at Tamil nadu in India and 80 control subjects with no occupational exposure of Pb. The serum tMg and albumin concentrations were estimated using diagnostic kit methods. Blood lead levels (BLLs) were estimated using atomic absorbtion spectrophotometer method. The fraction of cMg and iMg were calculated from serum tMg and albumin concentration among individual subjects. The BLLs was significantly (P<0.001) increased in the study group as compared to control. Serum tMg, cMg, iMg, % of iMg from tMg and % of iMg from cMg concentrations were not significantly decreased in the study group as compared to control. Pb-exposure was significantly associated with abnormal frequency distribution of serum iMg (P=0.048) and % of iMg from tMg (P=0.016). Smoking habit was significantly associated with cMg (P=0.039) and % of iMg from cMg concentration (P=0.018). The alcohol consumption was significantly (P=0.049) associated with cMg. The Pb-exposure and lifestyle factor such as smoking and alcohol consumption were associated with alteration of serum magnesium fractions.

Effect of Pb Exposure on Synaptic Scaling Through Regulation of AMPA Receptor Surface Trafficking.

Homeostatic synaptic plasticity (HSP) helps to stabilize the neuronal network activity, which is essential for optimal information coding. Synaptic scaling is a form of homeostatic plasticity that stabilizes neuronal firing in response to activity blockade. Lead (Pb) is a ubiquitous environmental neuro-toxicant and can impair the input-specific Hebbian type synaptic plasticity, but whether Pb exerts effects in HSP remains unknown. We previously reported that blocking L-type calcium channel induces synaptic scaling, which stimulates the synthesis of all-trans retinoic acid (RA) and the expression of GluA2-lacking α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor. Given Pb is a potent blocker of calcium channel, we hypothesized Pb may participate in synaptic scaling accompanied by RA synthesis and AMPA receptor trafficking. In this study, cultured hippocampal neurons were treated with Pb (1 μM 5 min, 15 min, 4 h, 24 h, and 10 μM 24 h) alone or in combination with tetrodotoxin (TTX, 1 μM, 24 h). The results showed that Pb alone, either at 1 μM or 10 μM, cannot induce synaptic scaling. But Pb participated in synaptic scaling when concurrent with TTX (10 μM Pb + 1 μM TTX, 24 h). Further results showed that surface heteromeric GluA1 and GluA2 AMPA receptors were increased in TTX+ Pb-induced synaptic scaling. In addition, RA was proved not to participate in TTX+ Pb-mediated synaptic scaling. Taken together, our work supported that TTX+ Pb could induce synaptic scaling and enhance synaptic accumulation of AMPAR GluA1 and GluA2 during synaptic up scaling. Our study would help for elucidation of the Pb-induced neuronal network instability mechanism.

The Effects of Lead (Pb) Exposure to Blood Pb Concentration and Hemoglobin Levels in Book Sellers and Street Vendors of Surakarta

Anemia is still a public health problem in the world and in Indonesia. WHO (2008) reported more than 75% of anemia in Asia is iron deficiency and 63.5% anemia in Indonesia is caused by lack of nutrition. Previous studies described that lead (Plumbum /Pb) can decrease hemoglobin levels. Sriwedari markets book sellers and Solo Wholesale Centers street vendors are susceptible populations exposed to Pb as a result of motor vehicle exhaust. Approximately 70% of Pb in vehicle exhausts emissions are emitted into the air. This study aimed to analyze the effects of Pb exposure on blood Pb concentration and hemoglobin levels. This study was a quantitative observational analytic study with cross sectional design conducted in 2015-2016 at Sriwedari Market. Samples were 97 respondents obtained through random sampling and Spearman correlation was used for data analysis. Result showed that there were association between Pb exposure in the air and blood Pb levels (p=0,000; r=0,606) and blood Pb levels and hemoglobin levels (p=0,000; r=-0,623)

Effect of Pb exposure on the cells and matrix of the intervertebral disc of rats

Degenerative spine diseases are common throughout the world. There are many factors that lead to these diseases. One of these exogenous factors may be Pb exposure. Most of the fundamental investigations about the negative effects of the Pb exposure have investigated the impact of high doses of Pb, while Pb exposure in low concentrations has been insufficiently studied. The nutrition of the intervertebral disc is provided by the vessels that grow into the vertebral bodies and the paravertebral tissue. This suggests the possibility that Pb penetrates from the bone to the intervertebral disc together with nutrients. This article reports an experimental study which was performed in rats aged 1.5 months (n = 40). Rats in the experimental group received lead acetate solution (230 mg of Pb per1 literof distilled water) as drinking water and the animals in the control group received distilled water for 10 weeks. In the isolated intervertebral discs, the content of Pb was determined by X-ray fluorescence spectrometry. The effect of lead on the structural organization of the intervertebral disc was investigated by light microscopy. The ultrastructural features of cells and the matrix intervertebral disc were studied by transmission electron microscopy. In the young animals after Pb exposure, a significant increase was found in the content of Pb in the intervertebral disc tissue, of 4.6 times compared to the control group. The histological analysis showed degenerative changes in the annulus fibrosus (AF) of the intervertebral disc. In the outer region cracks and defibration of the lamellae were observed. Large isogenic groups were detected in the inner region of the intervertebral disc. A decrease in the height by 12.2% in the outer parts and by 10% in the central part of the intervertebral disc was recorded. Also a reduction in the width of the lamellae by 8% was shown. Cell density of the annulus fibrous decreased by 12% and in the gelatinous nucleus pulposus (NP) by 24.2%. Electron microscopic analysis of the inner region of the AF of the intervertebral disc showed chondrocytes with electron-dense mitochondria, vacuolization of the cytoplasm, fragmented nuclei and destructive cavities. The matrix of the lamellae of the AF had a diverse electron density, so areas with high electron density of various sizes were observed. Collagen fibrils of the AF had blurred outlines, sometimes the transverse striation disappeared or it was irregular, which can indicate the matrix mineralization and possibly the accumulation of Pb in these areas. In the NP, the most notochordal cells revealed the formation of myelin figures. The effect of Pb at low concentration results in its accumulation in the tissues of the intervertebral disc of rats and causes degenerative changes in the intervertebral disc structure, leading to the reduction in the height of the intervertebral disc, decrease in the width of the lamellae and in cell density, thereby violating both the structures of matrix and cells. Future investigations of the collagen content of intervertebral disc after Pb exposure are needed.

Screening of damage induced by lead (Pb) in rye (Secale cereale L.) – a genetic and physiological approach

ABSTRACTThe fields in which lead (Pb) finds application in the modern world have increased dramatically in recent years. As a consequence of this intensive utilization of Pb, its toxicity tends to pose more and more environmental problems. The aim of this study was to evaluate the genotoxic potential of Pb and to characterize some physiological parameters in Secale cereale under Pb stress. Plants were subjected to different exposure levels of Pb (0, 100, 200 and 400 µmol/L) for two weeks. At the end of the experimental period, the effects of Pb exposure on the photosynthetic pigments content (chlorophyll a and b, total chlorophyll, chlorophyll a/b and carotenoids) and genetic material of S. cereale were studied. To evaluate the genotoxic effect of Pb, random amplified polymorphic DNA – polymerase chain reaction (RAPD-PCR) was employed. The obtained results showed alteration in the photosynthetic pigments content and RAPD-PCR profiles of S. cereale grown in the presence of Pb. The alterations in the RAPD-PCR profiles following Pb treatments appeared to be losses of normal bands and occurrences of new bands compared to unexposed plantlets. Overall, the content of chlorophyll a, chlorophyll b, total chlorophyll and carotenoids decreased by 6.68%, 6.08%, 2.89% and 8.57%, respectively, under severe Pb stress (400 µmol/L).

Lead Exposure Impairs Hippocampus Related Learning and Memory by Altering Synaptic Plasticity and Morphology During Juvenile Period.

Lead (Pb) is an environmental neurotoxic metal. Pb exposure may cause neurobehavioral changes, such as learning and memory impairment, and adolescence violence among children. Previous animal models have largely focused on the effects of Pb exposure during early development (from gestation to lactation period) on neurobehavior. In this study, we exposed Sprague-Dawley rats during the juvenile stage (from juvenile period to adult period). We investigated the synaptic function and structural changes and the relationship of these changes to neurobehavioral deficits in adult rats. Our results showed that juvenile Pb exposure caused fear-conditioned memory impairment and anxiety-like behavior, but locomotion and pain behavior were indistinguishable from the controls. Electrophysiological studies showed that long-term potentiation induction was affected in Pb-exposed rats, and this was probably due to excitatory synaptic transmission impairment in Pb-exposed rats. We found that NMDA and AMPA receptor-mediated current was inhibited, whereas the GABA synaptic transmission was normal in Pb-exposed rats. NR2A and phosphorylated GluR1 expression decreased. Moreover, morphological studies showed that density of dendritic spines declined by about 20% in the Pb-treated group. The spine showed an immature form in Pb-exposed rats, as indicated by spine size measurements. However, the length and arborization of dendrites were unchanged. Our results suggested that juvenile Pb exposure in rats is associated with alterations in the glutamate receptor, which caused synaptic functional and morphological changes in hippocampal CA1 pyramidal neurons, thereby leading to behavioral changes.

Early life lead exposure causes gender-specific changes in the DNA methylation profile of DNA extracted from dried blood spots.

In this paper, we tested the hypothesis that early life lead (Pb) exposure associated DNA methylation (5 mC) changes are dependent on the sex of the child and can serve as biomarkers for Pb exposure. In this pilot study, we measured the 5mC profiles of DNA extracted from dried blood spots (DBS) in a cohort of 43 children (25 males and 18 females; ages from 3 months to 5 years) from Detroit. Result & Discussion: We found that the effect of Pb-exposure on the 5-mC profiles can be separated into three subtypes: affected methylation loci which are conserved irrespective of the sex of the child (conserved); affected methylation loci unique to males (male-specific); and affected methylation loci unique to females (female-specific).

Lead-induced iron overload and attenuated effects of ferroportin 1 overexpression in PC12 cells

Lead (Pb) neurotoxicity has received renewed interest with the growing evidence that Pb contributes to Alzheimer’s disease (AD). However, the mechanism is not clear. In our previous study of long-term Pb exposure in vivo, a brain iron (Fe) overload induced by Pb was observedin elderly rats. It is well known that brain Fe overload is the mechanism of AD. Therefore, we have reason to believe that Pb induced Fe overload and caused neurodegenerative disease. However, the mechanism or route of Pb-induced Fe overload is unknown. In the current study, the effect of Pb exposure on Fe homeostasis in PC12 cells was determined at different Pb-exposure concentrations and periods with differing Fe exposure, and the role of ferroportin 1 (FP1), the sole iron efflux protein, in Pb-induced Fe metabolic disorders was further investigated. The results showed a Pb-induced cellular increase in Fe accompanying a decrease in the expression of FP1 in a concentration- and time-dependent manner in Pb-exposed PC12 cells. Furthermore, FP1 overexpression could attenuate Fe accumulation in Pb-exposed PC12 cells. These results indicated that FP1 might be a novel target to prevent cellular Fe accumulation induced by Pb exposure and subsequent neurotoxic consequences.

Effects of Pb exposure on oxidative stress biomarkers and plasma biochemistry in waterbirds from medina lagoon (Southern Spain)

Effects of Pb exposure on oxidative stress biomarkers and plasma biochemistry in waterbirds from medina lagoon (Southern Spain)