Good day Ma'am!
For the first question po:
First and foremost, rats are r-selected species—meaning that they have higher mortality and reproduction rates compared to k-selected species—such as humans. Rats reproduce more frequently because [1] they reach sexual maturity earlier, [2] they have shorter gestation periods (Hamid & Zakaria, 2012), and [3] they have efficient reproductive (e.g. spermatogenesis) capabilities (Johnson et al., 2014), among other reasons. Their spermatogenesis efficiency may be higher than other mammals such as humans because they can better adapt and survive in harsh environments, whereas other species are not as resilient, and respond negatively to even the slightest changes. With that said, humans may have the lowest efficiency of spermatogenesis because of several lifestyle- and environment-related factors such as poor diet choices (ingestion of preservatives and/or pesticides); obesity; smoking; and exposure to toxic chemicals and persistent environment pollutants. Because of these factors, effects on spermatogenesis (reversible) and sertoli cell number (potentially irreversible) become concerns (Sharpe, 2010).
For the second question po:
As reported, spermatogenesis is the process of development of sperm cells, while its efficiency is the estimated number of spermatozoa produced per day per gram of testicular parenchyma. By knowing its efficiency and understanding how it works, we can come up with male contraceptive methods, not only for humans but also for other animals.
One technique is through the exogenous administration of testosterone alone or along with gonadotropin-releasing hormone analog to suppress gonadotropins such as luteinizing hormone and follicle-stimulating hormone. This way, it acts through the negative feedback loop on the hypothalamic-pituitary axis, which ultimately reduces the endogenous testosterone release and prevents sperm production, thereby acting as a male contraceptive
To expound on this technique, low levels of LH lead to lower testosterone production by Leydig cells. Moreover, low levels of intratesticular testosterone and FSH suppress Sertoli cells, which facilitate the progression of germ cells to spermatozoa. Overall, these low testosterone levels will result in accelerated apoptosis, defects in spermiation, and sequestration of mature spermatozoa by Sertoli cells. In other words, this process will promote germ cell degeneration in males (Wang and Swerdloff, 2010).
Hope this answers your questions po!
References:
Hamid, H.Y. & Zakaria, Z.A.B. (2012, July 25). Reproductive Characteristics of the Female Laboratory Rat. African Journal of Biotechnology 12(19), pp. 2510-2514. https://academicjournals.org/article/article1380711761_Hamid%20and%20Zakaria.pdf
Johnson, L., Varner, D.D., Roberts, M.E., Smith, T.L., Keillor, G.E., & Scrutchfield, W.L. (2014). Efficiency of Spermatogenesis: A comparative approach. Animal Reproduction Science 60-61, pp. 471-480. https://doi.org/10.1016/S0378-4320(00)00108-1
Sharpe, R.M. (2010, May 27). Environmental/lifestyle effects on spermatogenesis. Phil. Trans. R. Soc. B3651697–1712
http://doi.org/10.1098/rstb.2009.0206
Wang, C. & Swerdloff, R.C. (2010, November 10). Hormonal Approaches to Male contraception. Current opinion in urology, 20(6), 520–524. https://doi.org/10.1097/MOU.0b013e32833f1b4a
