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Myelin protein zero and its antibody in serum as biomarkers of n -hexane-induced peripheral neuropathy and neurotoxicity effects

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Background Chronic exposure to n-hexane can lead to peripheral neuropathy that no effective treatment regimen could be applied presently. This study investigated whether myelin protein zero (P0) protein and its antibody could be used to distinguish n-hexane intoxication and protect workers from peripheral neuropathy. Methods We compared P0 protein and its antibody among three levels of n-hexane-exposed groups, which included 18 patients with n-hexane-induced peripheral neuropathy as case group, 120 n-hexane-exposed workers as n-hexane-exposed control group, and 147 non-hexane-exposed participants used as control group. ELISA method was applied to detect P0 protein and its antibody. Results P0 protein in serum was significantly higher in the case group and n-hexane-exposed control group in comparison with the control group (P<0.01). Compared with the n-hexane-exposed control group, the case group also had significant increase of P0 protein (P<0.01). After 6 months therapy, P0 protein was observed to decrease significantly in the case group (P<0.01). The P0 antibody in serum was significantly higher in the n-hexane-exposed control group than in the control group (P<0.01), but not significantly different between cases and controls. Conclusions P0 antibodies in serum may be a short-term effect biomarker for n-hexane exposure. P0 protein in serum may be an early effective biomarker for peripheral nerve neuropathy and its biological limit value needs investigation in the future study.
Title: Myelin protein zero and its antibody in serum as biomarkers of n -hexane-induced peripheral neuropathy and neurotoxicity effects
Description:
Background Chronic exposure to n-hexane can lead to peripheral neuropathy that no effective treatment regimen could be applied presently.
This study investigated whether myelin protein zero (P0) protein and its antibody could be used to distinguish n-hexane intoxication and protect workers from peripheral neuropathy.
Methods We compared P0 protein and its antibody among three levels of n-hexane-exposed groups, which included 18 patients with n-hexane-induced peripheral neuropathy as case group, 120 n-hexane-exposed workers as n-hexane-exposed control group, and 147 non-hexane-exposed participants used as control group.
ELISA method was applied to detect P0 protein and its antibody.
Results P0 protein in serum was significantly higher in the case group and n-hexane-exposed control group in comparison with the control group (P<0.
01).
Compared with the n-hexane-exposed control group, the case group also had significant increase of P0 protein (P<0.
01).
After 6 months therapy, P0 protein was observed to decrease significantly in the case group (P<0.
01).
The P0 antibody in serum was significantly higher in the n-hexane-exposed control group than in the control group (P<0.
01), but not significantly different between cases and controls.
Conclusions P0 antibodies in serum may be a short-term effect biomarker for n-hexane exposure.
P0 protein in serum may be an early effective biomarker for peripheral nerve neuropathy and its biological limit value needs investigation in the future study.

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