Mechanism of allyl chloride-induced cytoskeletal injury to nerve cells.
OBJECTIVE
To dissect the molecular mechanism of toxic neuropathy induced by allyl chloride (AC).


METHODS
Fluorescence molecular probe (Fura-2/AM), electron probe X-ray microprobe analysis (EPMA) and biochemical methods were used to determine the concentrations of cytosolic free Ca2+, the contents of intracellular Ca2+ percentage, Ca(2+)-free calmodulin (CaM), the activity of Ca2+/CaM-dependent protein kinase II (Ca2+/CaM-PK II), and cytoskeletal protein synthesis in chicken embryo brain cells induced by AC.


RESULTS
The contents of Ca2+ percentage, the concentrations of cytosolic free Ca2+, and the activities of Ca2+/CaM-PK II in the cells were increased significantly as AC was added (P < 0.01). However, the content of Ca(2+)-free CaM and the synthesis of cytoskeletal proteins were markedly decreased (P < 0.01).


CONCLUSIONS
The results suggest that one of the mechanism of AC-induced cytoskeletal injury in vitro might be related to the elevation of intracellular Ca2+, activated CaM and Ca2+/CaM-PK II.
Xie
K
K
Institute of Toxicology, Shandong Medical University, Jinan 250012, China.
Sun
K
K
Gao
S
S
Zhang
L
L
Zhang
M
M
D000498:Allyl Compounds / Q000633:toxicity*; D000818:Animals; D001370:Axonal Transport / Q000187:drug effects; D001921:Brain / Q000166:cytology; D002118:Calcium / Q000378:metabolism*; D017871:Calcium-Calmodulin-Dependent Protein Kinases / Q000378:metabolism*; D002147:Calmodulin / Q000378:metabolism; D002642:Chick Embryo; D003598:Cytoskeletal Proteins / Q000096:biosynthesis / Q000187:drug effects
D000498:Allyl Compounds; D002147:Calmodulin; D003598:Cytoskeletal Proteins; D017871:Calcium-Calmodulin-Dependent Protein Kinases; D002118:Calcium; C023698:allyl chloride