title: [Aluminium toxicosis causing transferable defects from exposed animals to their progeny in Caenorhabditis elegans].
abstract: 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 (2.5 micromol/L, 75 micromol/L, and 200 micromol/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 micromol/L aluminum exposed animals, the low-concentration (2.5 micromol/L) aluminium exposure caused severe defects of average survival days (20 d), body size [(1.12 +/- 0.02 ) mm, t = 14.55, P<0.01], brood size [(145 +/- 23), t = 30.62, P< 0.01], body bend [(29.8 +/- 3.0), t = 20.31, P<0.01], and head thrash, (95.8 +/- 6.2), t = 16.43, P < 0.01]. High-concentration aluminium exposure could further result in severe defects of generation time [75 micromol/L, (67.0 +/- 1.7 ) h, t = 8.92, P<0.01; 200 micromol/L, (70.7 +/- 1.5) h, t =15.13, P<0.01] and behavioral plasticity [75 micromol/L, (16.5 +/- 3.0)%, t = 27.11, P<0.05; 200 micromol/L, (23.5 +/- 4.0)%, t = 16.43, P<0.01]. 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.
  
  
  CONCLUSIONS
  The multi-biological defects caused by aluminium exposure might be largely transferred from exposed animals to their progeny in Caenorhabditis elegans.
authors.affiliation: Key Laboratory of Developmental Genes and Human Disease in Ministry of Education, Department of Genetics and Developmental Biology, Southeast University Medical School, Nanjing 210009, China. dayongw@seu.edu.cn
authors.forename: Da-yong
authors.initials: DY
authors.lastname: Wang
authors.forename: Yi-chao
authors.initials: YC
authors.lastname: Yang
authors.forename: Yang
authors.initials: Y
authors.lastname: Wang
mesh_terms: D000535:Aluminum / Q000633:toxicity*; D000818:Animals; D017173:Caenorhabditis elegans / Q000187:drug effects* / Q000235:genetics* / Q000254:growth & development; D064420:Drug-Related Side Effects and Adverse Reactions / Q000235:genetics*; D004781:Environmental Exposure; D004785:Environmental Pollutants / Q000633:toxicity; D017238:Genes, Helminth
chemical_list: D004785:Environmental Pollutants; D000535:Aluminum