“Effect of Endocrine Disrupting Chemicals on Germinal Vesicle Breakdown in Xenopus In Vitro,” by D. J. Fort, D. W. McLaughlin, R. L. Rogers, and B. O. Buzzard. Drug Chem. Toxicol. 25 (3), pp. 293–308, 2002.
Upon further review of our article cited above, we inadvertently did not cite the investigators (D. B. Pickford and I. D. Morris) who were responsible for the initial development of a germinal vesicle breakdown assay (GVBD) in Xenopus laevis as a means of studying endocrine disrupting agents properly. The following Erratum is provided to correct this error and includes the following revisions to the text.
Page 294, paragraph 3 is replaced with the following paragraph.
The maturation of the amphibian oocyte represents the final stage of oogenesis which ultimately prepares the oocyte for fertilization. Oocyte maturation is marked morphologically by germinal vesicle breakdown (GVBD),[24] and is induced by progesterone.[25] Thus, maturation of the oocyte could potentially be disrupted by EDCs. Disruption of oocyte maturation events in Rana pipiens[26] and X. laevis[24] by estradiol and a synthetic estrogen has been demonstrated previously. Thus, maturation of the oocyte could potentially be disrupted by EDCs. Pickford and Morris[27] previously hypothesized that progesterone-induced maturation of amphibian oocytes could be disrupted by environmental pollutants with anti-progestin activity. In this article, we further evaluate the use of a GVBD[27] assay for measuring EDCs in vitro.
Page 295, paragraph 2, line 16 is replaced with the following sentence.
Each of the test materials has also been found to induce abnormal development during early embryo-larval periods in the Frog Embryo Teratogenesis Assay—Xenopus (FETAX) model.[16]
Page 296, paragraph 4, line 1 is added.
Germinal Vesicle Breakdown (GVBD) Assay
The GVBD assay was performed as described by Pickford and Morris[27] with modification.
Page 303, paragraphs 2 and 3 are replaced with the following paragraph.
Exposure to environmental contaminants can adversely affect individuals, as well as, meta-populations of amphibians.[33] Most studies have focused on effects at the individual level. Extrapolating toxicological effects observed in individual specimens in the laboratory to effects at the meta-population level is extremely difficult and requires an adequate evaluation of adverse responses in the field. Negative effects at the meta-population level may be the result of multiple responses including lethal responses, sub-lethal responses, and modest changes in biochemical homeostatis.[27,32–34] Sub-lethal responses include malformation, growth reduction, and developmental delay. Changes in biochemical homeostasis in amphibians resulting from perturbation of critical aspects of the endocrine system, such as reproductive hormonal pathways and the thyroid axis also provide additional stress.
Amphibian reproduction can be perturbed at a myriad of different sites within the body including, the brain, pituitary, thyroid, gonad, and liver.[27] Of these systems, the gonads appear to be a primary site of action for many EDCs in several species. For example, abnormal ovaries in female juvenile alligators from Lake Apopka, Florida have been identified in earlier studies.[7,9,35–37] The biochemical and histopathological effects of organochlorine pesticides and polynuclear aromatic hydrocarbons (PAHs) on the ovaries of fish have been documented.[38,40] Thus, not only are EDCs capable of disrupting reproductive function by perturbing endocrine systems in adults, but also by inducing abnormalities in critical reproductive tissues.