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Manifestations of Neurotoxicity in Occupational Diseases
Published in Lucio G. Costa, Luigi Manzo, Occupatinal Neurotoxicology, 2020
Gases In carbon monoxide poisoning, the initial symptoms of headache, nausea, malaise, and lethargy may progress rapidly to loss of consciousness. This is commonly associated with high carboxyhemoglobin levels (>40% of the total hemoglobin). Carbon monoxide poisoning is one of the few examples of acute poisoning that may cause significant central nervous system damage in a delayed fashion.36 Clinically, delayed neurological sequelae may develop three days to three weeks after recovery from the initial exposure has appeared to be complete. Findings include mental deterioration, personality changes, speech disturbance, confusion, urinary/fecal incontinence, gait disturbance, weakness, and Parkinsonism. The pathogenesis of this particular syndrome is a matter of current controversy. During the acute stage, the effects of carbon monoxide in the brain have generally been related to functional hypoxia from impaired oxygen transport. However, patients who have never been significantly hypoxic may still develop delayed sequelae and, on the other hand, delayed neurotoxicity apparently does not develop in some patients despite their persistent initial coma. Postulated mechanisms of the delayed neurological sequelae consider (a) hypoxic-ischemic stress related to defective oxygen transport to the cells, (b) inhibition of cytochromes leading to impairment of mitochondrial electron transport in neural cells, (c) brain lipid peroxidation resulting from reperfusion injury, and (d) overstimulation of excitatory amino acid receptors.36 Other reported complications in carbon monoxide poisoning include hearing loss, retinal hemorrhages, and basal ganglion infarcts.
Physiological and pathophysiological implications of hydrogen sulfide: a persuasion to change the fate of the dangerous molecule
Published in Journal of the Chinese Advanced Materials Society, 2018
Jan Mohammad Mir, Ram Charitra Maurya
H2S exerts multifaceted and important effects in CNS through modulation of neurotransmission and neuromodulation. Glutamate is an important excitatory amino acid that functions as a neurotransmitter. Glutamate in mammalian brain is best known for its role in learning and memory, such as induction of long-term potentiated potential (LTP) and perception of pain. LTP is a memory consolidation process, which is ignited by a brief period of high-frequency presynaptic stimulation (5â100âHz), and this initial stimulation would enhance the postsynaptic response to subsequent presynaptic stimulation for many hours/days after the high-frequency tetanus. Abnormal glutamate metabolism can lead to excitatory neuronal injury. The neurological effects of glutamate are mediated by N-methyl-d-aspartate (NMDA) receptors in both central and peripheral nervous systems, with exceptions in the bone and pancreatic islet.[124] To date, a direct agonist role of H2S on NMDA receptors is unknown, but it has been found that at physiologically relevant concentrations H2S selectively enhances NMDA receptor-mediated currents and expedites the induction of hippocampal LTP in rats.[118, 125] On the other hand, high concentration of H2S would damage brain and lead to decreased learning and memory function.