Maternal lead exposure decreases the levels of brain development and cognition-related proteins with concomitant upsurges of oxidative stress, inflammatory response and apoptosis in the offspring rats

Hossain, Shahdat; Bhowmick, Sujan; Jahan, Sabrin; Rozario, Liza; Sarkar, Marzan; Islam, Saiful; Basunia, Mafroz Ahmed; Rahman, Azizur; Choudhury, Bazlul Karim; Shahjalal, Hussain Md.

doi:10.1016/j.neuro.2016.07.013

Cited by 64 publications

(22 citation statements)

References 53 publications

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“…Lead exposure is also linked with the depletion of brain GSH contents as indicated by the GSSG/GSSG + GSH ratio [45] . Studies have reported that lead-exposed animals showed a decrease in antioxidant defense mechanisms, such as catalase and superoxide dismutase, suggesting an increase in oxidative stress [9,46] . In vitro and in vivo studies have revealed that lead exposure may enhance the generation of ROS and increase the oxidative stress through changes in the antioxidant defense systems in animals [47] .…”

Section: Discussionmentioning

confidence: 99%

“…Occupational exposure to lead among industrial workers leads to the accumulation of this heavy metal in their body organs and tissues [7] . Experimental studies suggested that cholinergic dysfunction, glutamate receptor alteration and enhanced oxidative stress were all associated with lead-induced neurotoxicity [8,9] .…”

Section: Introductionmentioning

confidence: 99%

“…Metal chelating agents and natural antioxidants have been used to explore their beneficial effects in lead-induced neurotoxicity [9,15,16] . The increasing evidences support the beneficial effect of an increased intake of omega-3 fatty acids (omega-3FA) in a variety of neurodegenerative and neurological conditions [17] .…”

Section: Introductionmentioning

confidence: 99%

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Attenuation of Lead-Induced Neurotoxicity by Omega-3 Fatty Acid in Rats

Singh

Yadav

et al. 2017

Ann Neurosci

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Background: Lead is widely distributed in the environment and has been found to be associated with various health problems including neurodegenerative diseases. Purpose: In view of the increasing health risk caused by lead, this study has been carried out to investigate the neuroprotective effect of omega-3 fatty acid (omega-3FA) in lead-induced neurotoxicity in rats. Methods: Biochemical parameters including oxidative stress in brain regions, lead levels in blood and brain regions and histopathological examination of brain regions of rats were carried out in the present study. Results: Rats exposed to lead (lead acetate 7.5 mg/kg body weight p.o. for 14 days) caused a significant increase in the levels of lipid peroxidation, protein carbonyl content, ROS production and decreased the activities of glutathione peroxidase, superoxide dismutase and catalase in the cerebellum and cerebral cortex, respectively, as compared to controls. Abnormal histopathological changes and increase in the levels of lead in blood and brain were also observed as compared to controls. Co-treatment of lead with omega-3FA (750 mg/kg body weight p.o. for 14 days) decreased the levels of lipid peroxidation, protein carbonyl content, ROS production and increased the activities of glutathione peroxidase, superoxide dismutase and catalase and showed protection in the histopathological study as compared to rats treated with lead alone. Conclusions: The result of the present study shows that lead-induced oxidative stress and histopathological alteration in the brain region were significantly protected with co-treatment of lead and omega-3FA. This could be due to its strong antioxidant potential and metal-binding property.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Attenuation of Lead-Induced Neurotoxicity by Omega-3 Fatty Acid in Rats

Singh

Yadav

et al. 2017

Ann Neurosci

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“…There is currently no doubt about the serious effect of Pb-induced oxidative stress posing to the central nervous system (CNS). Pb exposure in rodents is linked to persistent alterations of brain derived neuronal factor (BDNF), β-amyloid (Aβ) aggregation, and oxidative damage accompanied by elevated apoptotic markers (Gu et al, 2011; Hossain et al, 2016). Childhood Pb poisoning continues to pose environmental public health challenges due to tightly association with impaired intelligence and growth (Wang et al, 2012; Mostafa et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Early-Life Exposure to Lead Induces Cognitive Impairment in Elder Mice Targeting SIRT1 Phosphorylation and Oxidative Alterations

Zhang

Wang

et al. 2017

Front. Physiol.

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Pb is a potential risk factor for cognition, mainly mediated by enhanced oxidative stress. Resveratrol, a natural polyphenol with crucial anti-oxidative property, is recently implicated in preventing cognitive deficits in normal aging and neurodegenerative disorders. Its beneficial effects have been linked to sirtuin 1(SIRT1) activation. The aim of this work is to investigate the possible linkage between alterations in Pb-induced oxidative damage and cognitive impairment by prolonged treatment of resveratrol. Male C57BL/6 mice were given Pb(Ac)2 treatment or deionized H2O for 12 weeks, and subjected to resveratrol gavage at the dose of 50 mg/kgBw•d or vehicle after Pb exposure. Results from biochemical analysis and immunohistofluorescence showed that Pb induced oxidative DNA damage and decreased cortical antioxidant biomarker. As expected, these abnormalities were improved by resveratrol treatment. Morris water maze test, Western blotting, immunohistofluorescence staining and RT-qPCR indicated that resveratrol ameliorated spatial learning and memory deficits with alterations in hippocampal BDNF-TrkB signaling, promoted nuclear localization and phosphorylation of hippocampal SIRT1, partly increased protein levels of AMPK and PGC-1α involving in modulation of antioxidant response in Pb-exposed mice. Our results support the hypothesis that resveratrol could attenuate Pb-induced cognitive impairment which was associated with activating SIRT1 via modulation of oxidative stress. Additionally, resveratrol also repressed the Pb-induce amyloidogenic processing with resultant decline in cortical Aβ1−−40. Noteworthy, such effects were not mediated by resveratrol treatment alone. These findings emphasize the potential of SIRT1 activator as an efficacious dietary intervention to downgrade the Pb-induced neurotoxic lesion.

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“…The levels of TNFα, PSD-95, SNAP-25, BDNF and TrkB proteins were determined by using indirect ELISA as previously described [39]. In brief, the multiwell plates were coated with 50 μg of cytosolic protein in a volume of 100 μl/well of carbonate buffer (pH 9.6) and incubated overnight at 4˚C.…”

Section: Tnfα Psd-95 Snap-25 Bdnf and Trkb Assaymentioning

confidence: 99%

Effects of <i>Syzygium cumini</i> Seed Extract on the Memory Loss of Alzheimer’s Disease Model Rats

Hossain¹,

Islam²,

Bhowmick³

et al. 2017

AAD

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Alzheimer's disease (AD) is the most prominent dementia-related disease and characterized by the presence of insoluble amyloid beta peptide (Aβ) fibers in or around the brain neurons of the affected person. Therefore, agent(s) capable of inhibiting brain amyloid deposition might delay the occurrence or retard the progress forwards of AD and related neurobehavioral symptoms.Here, we report whether, chronic oral administration of Syzygium cumini (locally known as Jam)-seed extract exerts protection against the progressive cognitive decline in the Aβ 1-40 -infused AD model rats. After 12 weeks of feeding with S. cumini seed extract (at 300 mg/kg BW), we evaluated the learning-related memory of the rats by 8-arm radial maze task, where we determined two types of memory errors, namely reference memory errors (RMEs) and working memory errors (WMEs). After completion of memory tests, rats were sacrificed and the levels of lipid peroxide (LPO), the Aβ 1-40 -burden, Aβ 1-40 -oligomers, proinflammatory TNFα, brain derived neurotrophic factor (BDNF), Tyrosine-kinase B (TrkB), postsynaptic-density protein 95 (PSD-95) and Synapse-associated protein (SNAP-25) were determined in the corticohippocampal tissues of the brain. In addition, in vitro antioxidative effects of S. cumini seed extract were evaluated. The oral administration of S. cumini extract significantly increased the memory-related learning ability of the AD model rats, concomitantly with reductions in the levels of corticohippocampal Aβ 1-40 -burden and Aβ 1-40 -oligomers. Furthermore, the extract suppressed the levels of TNFα and LPO in the corticohippocampal tissues of the AD rats and also the later in the plasma, suggesting an anti-oxidative and anti-inflammatory activities of the S. cumini extract in the brains of AD model rats. S. cumini extract also increased the levels of brain cognition and memory-related proteins, including BDNF, TrKB, PSD-95 and SNAP-25. We thus

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Maternal lead exposure decreases the levels of brain development and cognition-related proteins with concomitant upsurges of oxidative stress, inflammatory response and apoptosis in the offspring rats

Cited by 64 publications

References 53 publications

Attenuation of Lead-Induced Neurotoxicity by Omega-3 Fatty Acid in Rats

Attenuation of Lead-Induced Neurotoxicity by Omega-3 Fatty Acid in Rats

Early-Life Exposure to Lead Induces Cognitive Impairment in Elder Mice Targeting SIRT1 Phosphorylation and Oxidative Alterations

Effects of <i>Syzygium cumini</i> Seed Extract on the Memory Loss of Alzheimer’s Disease Model Rats

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Maternal lead exposure decreases the levels of brain development and cognition-related proteins with concomitant upsurges of oxidative stress, inflammatory response and apoptosis in the offspring rats

Cited by 64 publications

References 53 publications

Attenuation of Lead-Induced Neurotoxicity by Omega-3 Fatty Acid in Rats

Attenuation of Lead-Induced Neurotoxicity by Omega-3 Fatty Acid in Rats

Early-Life Exposure to Lead Induces Cognitive Impairment in Elder Mice Targeting SIRT1 Phosphorylation and Oxidative Alterations

Effects of &lt;i&gt;Syzygium cumini&lt;/i&gt; Seed Extract on the Memory Loss of Alzheimer’s Disease Model Rats

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Effects of <i>Syzygium cumini</i> Seed Extract on the Memory Loss of Alzheimer’s Disease Model Rats