Cadmium (Cd) is one of the most toxic heavy metals to which man can be exposed. Human Cd poisoning results mainly from occupational and environmental exposures. Cd affects cell cycle progression, proliferation, differentiation, DNA replication and repair, as well as apoptotic pathways. Acute intoxication is responsible for injuries to the testes, liver and lungs. Chronic exposure leads to obstructive airway diseases, emphysema, end-stage renal failures, diabetic and renal complications, deregulated blood pressure, bone disorders and immune-suppression. Cd is strongly associated with lung, prostate, kidney, liver, pancreas and stomach cancers, and, due to its oestrogen- like activity, it also plays role in the onset of breast cancer. The toxic effects of Cd on the central nervous system are still inadequately understood. On human neuroblastoma, Cd stimulates neurite outgrowth; on mouse gangliar and cortical neurons it induces degeneration and apoptosis. Cd seems to be involved in the pathogenesis of neurodegenerative diseases, as well as malformations. Among the chronic disease, Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disabling disorder of unknown etiology. Exposure to pollutants and viral infections can act as triggers. The symptomatology of ME/CFS suggests that this disorder could be related to alterations at the level of the temporal lobe. A recent study evidenced significant reductions in global gray matter volume in ME/CFS patients, linked to the reduction in physical activity. We noticed that Cd, as ubiquitous environmental pollutant, induces apoptotic and necrotic death in cortical neurons in culture. Therefore, we reasoned that Cd could represent one of the chemical triggers affecting cortical neurons and contributing to the onset as well as the perpetuation of ME/CFS. In order to assess the effects of Cd on cortical neurons in vivo, we developed an ultrasound imaging technique that allows to visualize the temporal cortex in alert subjects. The level of definition allows the study of the cellular layers of the cortex and is instrumental in assessing whether Cdexposed individuals show alterations of the layers of the temporal cortex as well as of the vascularisation of the meninges.
Cadmium toxicity, with particular regard to myalgic encephalomyelitis/chronic fatigue syndrome; application of transcranial sonography to the study of cadmium-induced neuronal damage
Gabriele Morucci;Jacopo Branca;
2012-01-01
Abstract
Cadmium (Cd) is one of the most toxic heavy metals to which man can be exposed. Human Cd poisoning results mainly from occupational and environmental exposures. Cd affects cell cycle progression, proliferation, differentiation, DNA replication and repair, as well as apoptotic pathways. Acute intoxication is responsible for injuries to the testes, liver and lungs. Chronic exposure leads to obstructive airway diseases, emphysema, end-stage renal failures, diabetic and renal complications, deregulated blood pressure, bone disorders and immune-suppression. Cd is strongly associated with lung, prostate, kidney, liver, pancreas and stomach cancers, and, due to its oestrogen- like activity, it also plays role in the onset of breast cancer. The toxic effects of Cd on the central nervous system are still inadequately understood. On human neuroblastoma, Cd stimulates neurite outgrowth; on mouse gangliar and cortical neurons it induces degeneration and apoptosis. Cd seems to be involved in the pathogenesis of neurodegenerative diseases, as well as malformations. Among the chronic disease, Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disabling disorder of unknown etiology. Exposure to pollutants and viral infections can act as triggers. The symptomatology of ME/CFS suggests that this disorder could be related to alterations at the level of the temporal lobe. A recent study evidenced significant reductions in global gray matter volume in ME/CFS patients, linked to the reduction in physical activity. We noticed that Cd, as ubiquitous environmental pollutant, induces apoptotic and necrotic death in cortical neurons in culture. Therefore, we reasoned that Cd could represent one of the chemical triggers affecting cortical neurons and contributing to the onset as well as the perpetuation of ME/CFS. In order to assess the effects of Cd on cortical neurons in vivo, we developed an ultrasound imaging technique that allows to visualize the temporal cortex in alert subjects. The level of definition allows the study of the cellular layers of the cortex and is instrumental in assessing whether Cdexposed individuals show alterations of the layers of the temporal cortex as well as of the vascularisation of the meninges.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
