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A steroid, testosterone was injected in female body which led to development of secondary sexual characters but these characters were not developed over night (Response was very slow). What could be possible explanation of this phenomenon

  1. a Steroid hormones produce a slow response because they do not have secondary messenger
  2. Slow response is due to lack of cell membrane receptors and amplification enzymes
  3. Movement of this hormone is very slow in blood
  4. None of the above

I think option 3 is correct because steroid hormones are hydrophobic in nature and cant be transported in the blood without the help of any carrier protein so this may be the reason but I am not sure about this..

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  • $\begingroup$ Read the title - it is completely valid. Answer to it. Then, lastly read the body. This should be reopened because I think we know too little about testosterone hormone and its effects in cell signalling and embryology. $\endgroup$ Commented Jul 8, 2014 at 14:41

2 Answers 2

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  1. Steroid hormones produce a slow response because they do not have secondary messenger
    It's true that steroids don't have secondary messengers because they don't need them - they can go directly into a cells nucleus and affect transcription there. This wouldn't slow down the response by much, however.
  2. Slow response is due to lack of cell membrane receptors and amplification enzymes
    This is just the inverse of the first option, which again isn't really a cause of slowing down the response. Steroids are amplified in that they act directly on DNA at the very first step of the synthesis pathways so don't need much amplification.
  3. Movement of this hormone is very slow in blood
    Again I don't think there is much to this option, the difference in speed of distribution of steroid and peptide hormones is likely to be minimal

This leaves us with:
4. None of the above

I would personally have gone with this answer. Steroids have a long time of action because they require the new transcription of genes that they activate. This process takes time and consistent doses are needed to maintain the effect.

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It may be important to consider the developmental stage of the "female body" as well. For instance, organizational vs. activational hypothesis--injecting testosterone during a critical period during development (it can be pre-natal, or during puberty) could produce permanent changes in secondary sexual characteristics and sex-specific behaviors; however, injecting testosterone after the organized system has "crystallized" (e.g. receptors are expressed in sex-specific regions, external genitalia is fully developed) may only induce temporary changes that may not be sex-specific.

As for a "female body" to develop secondary sex characteristics with testosterone injections--if these characteristics are "female" secondary sex characteristics (e.g. increased subcutaneous fat deposition in breasts in humans), it is likely that the machinery has already been organized (e.g. more "aromatase" converts testosterone to estrogen, or the location/density of androgen receptors affects sensitivity, or there is less androgen-binding protein to transport circulating testosterone), while if the secondary sex characteristics were "male" (e.g. laryngeal prominence) the testosterone injections happened during a critical development stage and/or were chronically administered (e.g. continuous administration, daily injections...).

Phoenix et al (a review cited above) did a cool experiment that might interest you.

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