Pregledni rad
https://doi.org/10.2478/v10004-007-0029-z
Axonal Degeneration and Neuropathy Target Esterase
Paul Glynn
Sažetak
This brief review summarises recent observations which suggest a possible mechanism for organophosphateinduced delayed neuropathy (OPIDN). Neuropathy target esterase (NTE) has been shown to deacylate endoplasmic reticulum (ER) membrane phosphatidylcholine (PtdCho). Raised levels of PtdCho are present in the brains of swiss cheese/NTE mutant Drosophila together with abnormal membrane structures, axonal and dendritic degeneration and neural cell loss. Similar vacuolated pathology is found in the brains of mice with brain-specific deletion of the NTE gene and, in old age, these mice show clinical and histopathological features of neuropathy resembling those in wild-type mice chronically dosed with tri-ortho-cresylphosphate. It is suggested that OPIDN results from the loss of NTE’s phospholipase activity which in turn causes ER malfunction and perturbation of axonal transport and glial-axonal interactions.
Ključne riječi
brain; carbamate; endoplasmic reticulum; organophosphate; phospholipid
Hrčak ID:
16535
URI
Datum izdavanja:
26.9.2007.
Posjeta: 2.795 *