秀丽线虫中铝暴露导致的多重毒害在世代间具有可转移特性

Aluminium toxicosis causing transferable defects from exposed animals to their progeny in Caenorhabditis elegans

目的研究铝暴露可能导致的多重毒性是否在世代间具有可传递特性。方法利用模式生物秀丽线虫对于铝（2．5、75、200μmol／L）暴露导致的寿命、发育、生殖、运动行为、行为可塑性等多种毒性及其在世代间的可传递性进行了研究。每个参数进行4组平行试验分析，寿命、发育、生殖与运动行为的分析每组20条线虫，行为可塑性的分析每组100条线虫。实验结果都用SPSS13．0软件进行分析。结果数据显示，铝暴露能导致线虫出现多种表型和行为缺陷。与0μmol／L浓度处理[平均存活天数，24d；体长（1．30±0．05）mm；后代数目（278±20）个；世代时间（64．0±1．2）h；身体弯曲频率（45．8±3．0）次；头部摆动频率（109．33±7．30）次；行为可塑性（3±4）％]相比，低浓度铝（2．5Ixmol／L）暴露即可导致平均存活天数（20d）、体长[（1．12±0．02）mm；t=14．55，P〈0．01]、后代数目[（145±23）个；t=30．62，P〈0．01]、运动行为[身体弯曲频率（29．8±3．0）次；t：20．31，P〈0．01。头部摆动频率（95．8±6．2）次；t=16．43，P〈0．01]等严重缺陷，而高浓度的铝暴露还可以导致世代时间[75μmol／L，（67．0±1．7）h；t=8．92，P〈0．01。200μmol／L，（70．7±1．5）h；t=15．13，P〈0．01]与行为可塑性[75μmol／L，（16．5±3．0）％；t=27．11，P〈0．05。200μmol／L，（23．5±4．0）％；t=16．43，P〈0．01]等的严重缺陷。而且，大部分高浓度铝暴露导致的缺陷可以从暴露当代传递到后代，使后代仍然呈现出严重表型与行为缺陷。在这些后代中，各表型与行为缺陷只能得到有限的恢复（如体长、后代数目与运动行为），或没有明显的恢复（如高浓度铝暴露引起的寿命缺陷）。尤其是，铝引起的世代时间缺陷在子代中会变得更为严重。结论在秀丽线虫中，铝暴露导致的针对表型与行为的多重毒害在很大程度上可以从当代动物传递到后代个体中。

Objective To study the possibly transferable properties of multi-biological toxicities caused by aluminium exposure from exposed animals to their progeny. Methods Multi-biological toxicities in aluminium （2. 5μmol/L,75μmol/L,and 200μmol/L） exposed animals and their progeny were analyzed by using model organism Caenorhabditis elegans. Endpoints of lifespan, development, reproduction, locomotion behavior and behavioral plasticity were selected for the assay of multiple toxicities and their transfer properties. Four groups of experiments were performed for each endpoint assay. Twenty animals were used for assay of lifespan, development, reproduction and locomotion behaviors, and 100 animals were used for assay of behavioral plasticity in each group experiment. The data were performed for statistical analysis using SPSS 13.0 software. Results Our data suggest that the aluminium exposure could result in multi-biological defects of phenotypes and behaviors. As compared to those average survival days, 24 d, body size, （ 1.30 ± 0.05） mm; brood size, （278 ±20） ; generation time（64.0 ± 1.2）h; body bend, （45.8 ±3.0） times, head thrash, （ 109. 33 ± 7.30） times, behavioral plasticity （ 3 ± 4） % in 0 μmol/L aluminum exposed animals, the low-concentration （2. 5 μmol/L ） aluminium exposure caused severe defects of average survival days （20d）,body size[（1.12 ±0.02 ） mm,t=14.55,P〈O. O1],brood size[（145±23）,t=30.62,P〈 0. 01],bodybendI（29.8±3.0）,t=20.31,P〈0.011,and head thrash,（95.8 ±6.2）,t=16.43,P〈 O. 01 ]. High-concentration aluminium exposure could further result in severe defects of generation time E75 μmol/L,（67.0±1.7 ）h,t=8.92,P〈0. O1; 200 μmol/L,（70.7±1.5） h,t=15.13,P〈0. 01]and behavioral plasticity [ 75 μmol/L, （ 16.5 ± 3.0 ）% , t = 27. 11, P 〈 O. 05 ; 200 μmol/L, （23.5 ± 4.0 ）% , t = 16.43,P 〈 0. 011. Moreover, most of these toxicities caused by high-concentration aluminium exposure could be transferred from exposed animals to their progeny. In progeny animals, the phenotypic and behavioral defects might be only partially （ such as body size, brood size, and locomotion behaviors ） or very slightly （such as the lifespan defects induced by high concentrations of aluminium exposure） rescued. Especially,the generation time defects induced by aluminium exposure would become more severe in progeny animals than in their parents. Conelusion The multi-biological defects caused by aluminium exposure might be largely transferred from exposed animals to their progeny in Caenorhabditis. elegans.