Acrylamide exposure impairs blood-cerebrospinal fluid barrier function
Xue Yao1, Yanshu Zhang1, Licheng Yan2, Lin Yao2, Weijun Guan3, Fanxu Zeng1, Fuyuan Cao2, Yanshu Zhang1
1 College of Public Health, Hebei United University, Tangshan, Hebei Province
2 Experimental Animal Center, Hebei United University, Tangshan, Hebei Province
3 Key Laboratory of Hebei Health and Safety on Coal Industry, Hebei United University, Tangshan, Hebei Province
College of Public Health, Hebei United University, Tangshan, Hebei Province
Ph.D., College of Public Health, Hebei United University, Tangshan 063000, Hebei Province
Source of Support: Funding: This study was supported by State Key Development Program for Basic Research of China, No. 2012CB525002 and the National Natural Science Foundation of China, No. 30771823.
Yao X, Yan LC, Yao L, Guan WJ, Zeng FX, Cao FY, Zhang YS. Acrylamide exposure impairs blood-cerebrospinal fluid barrier function. Neural Regen Res. 2014;9(5):555-560., Conflict of Interest: None
Previous studies show that chronic acrylamide exposure leads to central and peripheral neuropathy. However, the underlying mechanisms remained unclear. In this study, we examined the permeability of the blood-cerebrospinal fluid barrier, and its ability to secrete transthyretin and transport leptin of rats exposed to acrylamide for 7, 14, 21 or 28 days. Transthyretin levels in cerebrospinal fluid began to decline on day 7 after acrylamide exposure. The sodium fluorescein level in cerebrospinal fluid was increased on day 14 after exposure. Evans blue concentration in cerebrospinal fluid was increased and the cerebrospinal fluid/serum leptin ratio was decreased on days 21 and 28 after exposure. In comparison, the cerebrospinal fluid/serum albumin ratio was increased on day 28 after exposure. Our findings show that acrylamide exposure damages the blood-cerebrospinal fluid barrier and impairs secretory and transport functions. These changes may underlie acrylamide-induced neurotoxicity.