Developmental lead (Pb)-induced deficits in hippocampal protein transl | NDT #Protein_TranslationDecember 7, 2018
Faraz Ahmad, 1 Mohammad Salahuddin, 2 Khaldoon Alsamman, 3 Abdulaziz A AlMulla, 4 Khaled F Salama 4
1 School of Life Science, BS Abdur Rahman Crescent Institute of Science & Technology, Vandulur, Chennai 600048, India; 2 Animal House Department, Institute for Research and Medical Consultations, Imam Abdurrahman Bin Faisal University, Dammam 31441, Saudi Arabia; 3 Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Imam Abdurrahman Bin Faisal University, Dammam 31441, Saudi Arabia; 4 Department of Environmental Health, College of Public Health, Imam Abdurrahman Bin Faisal University, Dammam 31441, Saudi Arabia
Background: Lead (Pb) is a persistent environmental neurotoxin and its exposure even in minute quantities has been known to induce neuronal defects.
The immature brain is singularly sensitive to Pb neurotoxicity, and its exposure during development has permanent detrimental effects on the brain developmental trajectory and neuronal signaling and plasticity, culminating into compromises in the cognitive and behavioral attributes which persists even later in adulthood.
Several molecular pathways have been implicated in the Pb-mediated disruption of neuronal signaling, including elevated oxidative stress, alterations in neurotransmitter biology, and mitochondrial dysfunction.
Moreover, we evaluated the therapeutic effects of ascorbic acid supplementation against Pb-induced deficits in synapse-localized protein translation.
Results: We observed a significant loss in the rates of de novo protein translation in synaptoneurosomes of Pb-exposed pups compared to age-matched control pups.
Moreover, the deficit in activity-dependent synaptic protein translation was found to correlate significantly with the increase in the blood Pb levels.
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