) The authors thank Wenzhou center for disease control and prevention (Zhenjiang province, ABT-199 cost China) for recruiting the volunteers. “
“The authors regret that the following was not included in the Acknowledgment: This paper was supported by the SMART Research Professor Program of Konkuk University. The authors would like to apologize for any inconvenience caused. “
“Tellurium (Te) applications in electronics, optics, batteries and mining industries have expanded during the last few years, leading

to an increase in environmental Te contamination, thus renewing biological interest in Te toxicity. The main target sites for Te toxicity are the kidney, nervous system, skin, and the fetus (hydrocephalus) (Taylor, 1996). Nevertheless, several reports Selleckchem Akt inhibitor support that inorganic and organic

tellurium compounds are highly toxic to the CNS of rodents (Maciel, 2000). Organotellurium compounds lead to degradation of the myelin sheath and consequently a transient demyelination of peripheral nerves (Nogueira et al., 2004). Neurofilaments (NF) are the primary intermediate filaments (IF) in mature neurons. They assemble from three subunit polypeptides of low, medium and high molecular weight, NF-L, NF-M, and NF-H, respectively. This process is finely regulated via phosphorylation of lysine–serine–proline (KSP) repeats in the carboxyl-terminal domain of NF-M and NF-H. The majority of KSP repeats in rat-mouse NF tail domains are phosphorylated by mitogen-activated protein kinases (MAPK) (Veeranna et al., 1998); glycogen synthetase kinase 3 (GSK3) (Guan et al., 1991); p38MAPK (Ackerley et al., 2004;) and c-Jun N-terminus kinase 1 and 3 (JNK1/3) (Brownlees et al., 2000). Otherwise, phosphorylation sites located on the amino-terminal domains of the three NF subunits are the targets of second messenger-dependent

protein kinases, such as cAMP-dependent protein kinase (PKA), Ca2+/calmodulin-dependent protein kinase (PKCaM) and Ca2+/diacylglycerol-dependent protein kinase (PKC) (Sihag and Nixon, 1990). The correct formation of an axonal network of NF is crucial for the establishment and maintenance of axonal caliber and consequently for the optimization of conduction velocity. Glial fibrillary P-type ATPase acidic protein (GFAP) is the IF of mature astrocytes. GFAP expression is essential for normal white matter architecture and blood–brain barrier integrity, and its absence leads to late-onset CNS dysmyelination (Liedtke et al., 1996). There is now compelling evidence for the critical role of the cytoskeleton in neurodegeneration (Lee et al., 2011). Moreover, aberrant NF phosphorylation is a pathological hallmark of many human neurodegenerative disorders as well as is found after stressor stimuli (Sihag et al., 2007).