【摘要】：本研究旨在探討甲醛導(dǎo)致機(jī)體神經(jīng)系統(tǒng)病變的具體機(jī)制。選用雄性Balb/c小鼠為研究對(duì)象,動(dòng)態(tài)吸入甲醛方式染毒7天,每天8 h,甲醛濃度分別為0、0.5、3.0 mg/m3,同時(shí)設(shè)置一氧化氮合酶(nitric oxide synthase,NOS)拮抗劑(NG-monomethylL-arginine,L-NMMA)組,該組小鼠同時(shí)進(jìn)行3.0 mg/m3甲醛染毒。染毒結(jié)束后,用試劑盒檢測(cè)小鼠大腦皮層、海馬和腦干中環(huán)磷酸腺苷(cyclic adenosine monophosphate,cAMP)、環(huán)磷酸鳥苷(cyclic guanine monophosphate,cGMP)、一氧化氮(nitric oxide,NO)含量和NOS活性的變化。結(jié)果顯示,與對(duì)照組相比,小鼠大腦皮層和腦干中cAMP含量在0.5 mg/m3染毒組顯著升高(均P0.05),但是在3.0 mg/m3染毒組顯著降低(P0.05),海馬中cAMP含量?jī)H在3.0 mg/m3染毒組出現(xiàn)顯著降低(P0.05);與對(duì)照組相比,L-NMMA拮抗組小鼠cGMP和NO含量分別在海馬和大腦皮層中顯著上升(均P0.01),而cAMP含量和NOS活性在不同腦區(qū)中無顯著變化。與3.0 mg/m3染毒組相比,L-NMMA拮抗組不同腦區(qū)中cAMP含量均顯著上升(均P0.05),NOS活性顯著下降(P0.05或P0.01);大腦皮層和腦干中的cGMP含量以及腦干中的NO含量亦出現(xiàn)顯著性變化(P0.05或P0.01)。以上結(jié)果提示,甲醛暴露的神經(jīng)系統(tǒng)毒性作用與NO/cGMP信號(hào)轉(zhuǎn)導(dǎo)通路和cAMP信號(hào)通路存在一定的關(guān)系。
[Abstract]:The purpose of this study was to explore the mechanism of formaldehyde causing neuropathy. Male Balb/c mice were exposed to formaldehyde for 7 days and 8 hours a day. The concentration of formaldehyde was 0.5 mg/m3, and 3.0 mg/m3, respectively. The mice were treated with (nitric oxide synthase,NOS antagonist (NG-monomethylL-arginine,L-NMMA). The mice were exposed to 3.0 mg/m3 formaldehyde at the same time. After exposure, the changes of (cyclic adenosine monophosphate,cAMP, (cyclic guanine monophosphate,cGMP, nitric oxide,NO and NOS activity in cerebral cortex, hippocampus and brainstem of mice were detected by using the kit. The contents of cyclic guanosine monophosphate (cyclic guanine monophosphate,cGMP) and the content of cyclic adenosine monophosphate (nitric oxide,NO) in hippocampus and brain stem were measured. The results showed that, compared with the control group, The content of cAMP in cerebral cortex and brainstem of mice increased significantly at 0.5 mg/m3 (P0.05), but decreased significantly in 3.0 mg/m3 group (P0.05), and cAMP content in hippocampus decreased only in 3.0 mg/m3 group (P0.05). Compared with control group, L-NMMA antagonistic group was smaller than control group. The contents of cGMP and NO increased significantly in hippocampus and cerebral cortex respectively (P0.01), but the content of cAMP and the activity of NOS did not change in different brain regions. Compared with 3.0 mg/m3 group, cAMP content in different brain regions of L-NMMA antagonistic group increased significantly (P0.05 or P0.01), and cGMP content in cerebral cortex and brainstem and NO content in brainstem also showed significant changes (P0.05 or P0.01). These results suggest that the neurotoxicity of formaldehyde exposure is related to NO/cGMP signal transduction pathway and cAMP signaling pathway.
【作者單位】： 華中師范大學(xué)生命科學(xué)學(xué)院遺傳調(diào)控與整合生物學(xué)湖北省重點(diǎn)實(shí)驗(yàn)室;
【基金】：supported by the Key Project of National Natural Science Foundation of China(No.51136002) the Open Project Program of Hubei Key Laboratory of Genetic Regulation and Integrative Biology,China(No.GRIB201501)
【分類號(hào)】：R114

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