Environmental Impacts on Sexual Development Flashcards

1
Q

What did industrial effluents do to fish and what does this imply?

A

Male fish upregulated vitellogenin which is an egg component normally only found in the female. It implied estrogens in industrial effluent.

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2
Q

How was this similar in aligators?

A

Genital abnormalities in neonatal alligators in florida everglades. (Places close to industrial effluents)

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3
Q

Why are alligators not a good model for genital malformations in humans?

A

Their sex determination is temperature dependent whereas in humans it is dependent on hormones dependent on SRY - so confounding effects??

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4
Q

What are the clinical trends in:

a) birth defects
b) sperm
c) testicular cancer

A

a) Increasing cryptorchidism and hypospadias
b) Increased incidence of Decreased sperm counts (oligozoospermia). This is thought to be linked to decreased fetal sertoli cells.
c) Decreased sperm counts are a risk factor for testicular cancer and vica versa. Increased incidence of this reflects abnormal development of fetal germ cells. It can also reflect testicular dysgenesis.

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5
Q

How are sertoli cells involved in spermatogenesis?

A

They provide graded microenvironments for the sperm. Their number determines the spermatogenic capacity of the testes. Estrogens or environmental estrogen mimics are toxic to sertoli cells.

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6
Q

What are the different sources of environmental estrogens?

A
The pill
Phytoestrogens (soy)
Polychlorobisphenols (PCB)
phthalates 
   - both the above are plasticizers)
anionic detergents
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7
Q

What is testicular dysgenesis?

A

Disorder of testes histology due to abnormal sertoli/leydig cell development and therefore poorly formed seminiferous tubules.

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8
Q

What is its link to testicular cancer?

A

It is commonly seen in the contralateral testis of men with unilateral testicular cancer.

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9
Q

What are the main characteristics of it?

A

Immature/lack of sertoli cells

Foci of leydig cell hyperplasia.

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10
Q

What was the effect of dibutyl phthalate on the pups of treated pregnant rats?

A

Only 2/10 fertile
6/10 hypospadias
all were cryptorchid.

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11
Q

How was testicular descent related to testicular weight?

A

Those that descended displayed catch up growth.

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12
Q

Why would there be leydig cell hyperplasia?

A

Reduced testosterone production would lead to high LH levels (as no negative feedback) so Leydig cells would hyperplasia to catch up.

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13
Q

How did DBP affect the seminiferous tubules?

A

Sertoli cell only tubule with no lumen - very little spermatogenesis.

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14
Q

Why would incomplete formation of seminiferous tubules be very bad?

A

There would be a lack of blood-testes barrier leading to inflammation.

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15
Q

Summarise the primary defects in TDS.

A

Incomplete sertoli cells formation
Lack of germ cells but inclusion of Leydig cells in STs.
Decreased leydig cell testosterone output and subsequent leydig cell hyperplasia, cryptorchidism and/or hypospadias.

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16
Q

How did sewage sludge affect lambs born to grazing sheep?

A

It had an adverse impact on ovarian development, hypothalamic development

  • Decreased Kiss-1 mRNA
  • Decreased hypothalamic kisspeptin