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Manifestations of Neurotoxicity in Occupational Diseases
Published in Lucio G. Costa, Luigi Manzo, Occupatinal Neurotoxicology, 2020
Unfortunately, mechanisms of toxicity and primary cellular and subcellular targets have been elucidated for only a limited number of neurotoxicants. A number of processes are evidently implicated. Changes in the neuronal, axonal, myelin, or muscle membrane structure can impair excitability and impede impulse transmission. Alterations in protein, fluid content, or ionic exchange capability of the membrane may provoke swelling of neurons and astrocytes, damage to capillary endothelium, or increase extracellular fluid. Toxic effects on specific neurotransmitter mechanisms block neurotransmitter access to post-synaptic receptors, produce false neurotransmitter effects, or alter the synthesis, storage, release, re-uptake, or enzymatic inac-tivation of natural neurotransmitters.61
Sex differences in 123I-mIBG scintigraphy imaging techniques in patients with heart failure
Published in Expert Review of Medical Devices, 2023
Miriam Conte, Maria Silvia De Feo, Viviana Frantellizzi, Arianna Di Rocco, Alessio Farcomeni, Flaminia De Cristofaro, Ricci Maria, Antonio Rosario Pisani, Giuseppe Rubini, Giuseppe De Vincentis
The scintigraphy with 123I-mIBG could be a potentially useful tool to stratify patients with heart failure. It is possible to determine the density and the function (that is the turnover) of presynaptic norepinephrine (NE) receptors through the cardiac uptake on late 123I-mIBG images. Since mIBG is an analog of the false neurotransmitter guanethidine, it is not degraded and catabolized back in the presynaptic terminals after the uptake in the presynaptic terminal by NET-1 (NE transporter 1 or also called uptake-1). It accumulates in presynaptic vesicles and gives information about the possible denervation grade in the myocardium [10] which is typical of chronic heart failure (CHF).