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. Author manuscript; available in PMC: 2012 Dec 1.
Published in final edited form as: Reprod Toxicol. 2011 Sep 24;32(4):472–483. doi: 10.1016/j.reprotox.2011.09.006

Table 3. Summary of Neonatal DES-Induced Disruption Endpoints and Attributes.

Mechanistic Attributes
Disruption Endpoint Early (E) or Late (L)a Transient (T) or
Persistent (P)b 		Direct (D) or Indirect
(I)c
Uterine and Cervical
Dimensions		 E P D
Salpingitis L P I
Polyovular Follicles
(POF)		 E T D
Cystic Follicles L P I
Hypospadias L P D
Endocrine Status E & L P D & I
Endometrial
Hyperplasia/Dysplasia		 E P D
Lack of Corpora
Lutea		 L P ?
a

Indicates whether the disruption endpoint emerged either prepubertally (early, E) or postpubertally (late, L).

b

Indicates whether presence of the disruption endpoint waned after it first emerged (transient, T) or continued and/or progressed thereafter (persistent, P).

c

The characterization of whether the disruption endpoint is due either to a direct (D) mechanism that involves immediate DES-induced alterations in development of the perinatal tissue/organ or to an indirect (I) mechanism that involves altered development and function of the hypothalamus and/or pituitary which, in turn, results in altered gonadotropin-regulated function of the mature ovary.