Premium
Effects of pond water, sediment and sediment extract samples from new hampshire, usa on early Xenopus development and metamorphosis: comparison to native species
Author(s) -
Fort Douglas J.,
Rogers Robert L.,
Paul Robbin R.,
Miller Mark F.,
Clark Patrick,
Stover Enos L.,
Yoshioko Joy,
Quimby Fred,
Sower Stacia A.,
Reed Karen L.,
Babbitt Kimberly J.,
Rolland Rosalind
Publication year - 2001
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.740
Subject(s) - metamorphosis , maldevelopment , amphibian , biology , larva , xenopus , resorption , sediment , embryogenesis , embryo , in ovo , ecology , endocrinology , fishery , paleontology , biochemistry , gene
In an effort to assess potential ecological hazards to amphibian species in selected regions within New Hampshire, the traditional Frog Embryo Teratogenesis Assay—Xenopus (FETAX), a 14‐/21 day tail resorption thyroid disruption assay and >30 day limb development tests were conducted with representative surface water and sediment samples. Two separate sets of samples collected from five sites were evaluated. The primary objectives of the study were to determine if samples were capable of inducing early embryo‐larval maldevelopment, to determine if maldevelopment included limb defects, to determine if thyroxine co‐administration altered the rates of limb malformation and to evaluate the impact of the samples on growth rates, developmental progress and metamorphic climax. Results from these studies suggested that pond water and sediment extract samples, but not whole sediment samples, from B2, FW, LP and W ponds were capable of inducing abnormal early embryo‐larval development. In addition, water samples from B2 and W ponds induced significant abnormal hindlimb development. Some abnormal forelimb development was noted in the tail resorption studies, but not to the same extent as the hindlimbs. Each of the water samples induced appreciable developmental delay, including the paired reference site B1, which could be reversed by the addition of exogenous thyroxine. Copyright © 2001 John Wiley & Sons, Ltd.