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Absence/Excess of Hormones in Determination of Phenotypic Sex

GOAL: To describe the control of sexual differentiation and describe the consequences of defective regulatory mechanisms.

Objective:
To describe the genetic and hormonal factors controlling differentiation of the gonads, reproductive tract and external genitalia.

 

-What would be the potential consequences of a defect in synthesis or action of
 testosterone and/or mullerian inhibiting hormone in male fetuses?
-What would be the potential consequences of a defect in synthesis or action of
 testosterone in female fetuses?
-What would be the potential consequences of excess estrogen in male and
 female fetuses?

 

The Wolffian ducts would fail to develop. In this case, the mullerian ducts would nonetheless degenarate because Mullerian Inhibiting Hormone MIH continues to be produced. The external genitalia are incompletely developed and appear to be female. The Wolffian ducts would develop and the mullerian ducts would develop. The external genitalia would develop normally.

The wolffian ducts and external genitalia fail to develop due to the lack of testosterone and the mullerian ducts develop due to the lack of mullerian inhibiting hormone. The mullerian ducts develop normally and, depending on the time of exposure to excess androgens the wolffian ducts could also be partially developed.

The external genitalia appear to be male. Maternal ingestion of synthetic progestins, which have some androgenic activity, or testosterone during pregnancy causes masculinization of the external genitalia of neonatal females, usually manifest as fusion of the labioscrotal folds and clitoromegaly. There can be anomalies in development of the reproductive tract noticeable at birth in either the male or the female.

Moreover, exposure of the female reproductive tract to excess estrogens in utero can result in malignancies in the estrogen-responsive tissues later in life.