| Objective Studies show that lead exposure can affect the iron content in the central nervous system, which is essential for the growth, metabolism and function of the brain.Study on changes of the iron release protein in the brain tissue of rats after lead exposure has not been reported.The current study is to investigate the role of ferroportin1 in nerve injury of lead exposed offspring rats on the growth and development period. The finding will provide a theoretical basis for the mechanism of injury after lead exposure.Method 1 The experimental animal and grouping: 20 SD pregnancy rats were randomly divided into 2 groups. Pregnancy rats in control group were given 0.05%sodium acetate in drinking and pregnancy rats in lead exposure group were given 0.05%lead acetate in drinking. Since the first day, pregnant rats were given 0.05% lead acetate in drinking. At PND21, offspring rats were weaing and fread with 0.05% Pb Ac until PND42.2 Recording the volume of drinking water, activity, diet, and measuring body weight of offspring rats.3 The water maze test was used to measure the learning and memory function of offspring rats.4 ICP-MS was applied to detect lead and iron content in cortex and hippocampus. 5 Application of ELISA method to detect the content of s Tf R,TIBC, ferritin, ferroportin1(FPN1), hephaestin(HP), ceruloplasmin(CP).6 HE staining was used to observe pathological changes of in rat brain tissue.7 Perl’s iron staining was used to show the distribution of iron. 8 Real-time PCR was used to the measure the FPN1 m RNA, HP m RNA, CP m RNA expression.Statistical analysis: All data were showed sx±. The statistics methods include t-test, correlation analysis. P<0.05 was considered statistically significant.Results 1 The damage induced by lead exposure of different developmental stages of offspring rats. 1) The escape latencies of PND21 and PND42 in lead exposure group were longer than that of control group. The number of crossing the platform in lead exposure group decreased. 2) HE staining showed that the lead exposure induced the number of neuron degeneration reduced and necrosis, some neurons arranged in disorder of hippocampus and cortical neurons compared with control group. 3) Lead content of hippocampus, cortex of PND1, PND21, PND42 rats of lead exposure group were higher than those in control group,the difference was statistically significant(P<0.05). 2 Effects of lead exposure on iron content in the cortex and hippocampus of rats. 1) Iron content of cortex of PND1 rats of lead exposure group were(7.231±1.640) μg/g,(34.285±5.671)μg/g,(47.628±8.741) μg/g,1.42,1.25 and 1.30 folds of those in the control group.Iron content of hippocampus of PND1, PND21, PND42 rats of lead exposure group were(64.23±18.24) μg/g,(103.11±21.35) μg/g,(57.70±9.81) μg/g, 1.53, 1.22 and 1.53 folds of those in the control group. 2) A large number of iron deposition in the hippocampus, cortex tissue of PND1, PND21, PND42 rats in lead exposure group. 3)Ferritin levels in hippocampus of PND1, PND21, PND42 rats of lead exposure group were(6.98 ± 0.88) μg/g protein,(5.41 ± 1.06) μg/g protein,(5.28 ± 0.88) μg/g protein,which were significantly higher than those in control group(P<0.05). Correlation analysis results showed that iron content were positively correlated with lead content,navigation time in pups’ cortex and hippocampus by lead exposure. 3 Effects of lead exposure on offspring of iron release proteins. 1) FPN1 levels in hippocampus of PND1 rats in lead exposure group were(4.45±0.82) ng/g protein, FPN1 levels in hippocampus of PND42 rats in lead exposure group were(2.68±0.67) ng/g protein, lower than those in control group(P<0.05). FPN1 levels in cortex of PND21 rats in lead exposure group were(3.82 ±0.27) ng/g protein lower than those in control group,(P<0.05). Real-time PCR results showed that lead exposure group, FPN1 m RNA expression in the cortex,hippocampus of PND1, PND21, PND42 rats were lower than those in control group. 2)HP levels in hippocampus of PND42 rats in lead exposure group were lower than those in control group,(P<0.05). Real-time PCR results showed that lead exposure group, HP m RNA expression in the hippocampus of PND1, PND21, PND42 rats were lower than those in control group. HP m RNA expression in the cortex of PND1, PND42 rats were lower than those in control group. 3) CP levels in hippocampus of PND1, PND21,PND42 rats in lead exposure group were(49.05±13.29) ng/g protein,(45.91±7.52) ng/g protein,(32.33±8.61) ng/g protein,lower than those in control group,(P<0.05). Realtime PCR results showed that lead exposure group, CP m RNA expression in the cortex,hippocampus of PND1, PND21, PND42 rats were lower than those in control group.Conclusion 1 The imbalance of iron homeostasis caused by lead exposure during the growth and development is related to the development of central nervous system.2The lead exposure during the growth and development lead to the decrease of the expression of FPN1, and FPN1 involved in the development of central nervous system caused by lead exposure. |
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