Introduction
During infancy, the majority of ova in ovaries are found within non-mounting follicles, which are usually small in size. However, follicular mounting starts when oocyte begins to replicate, increasing in numbers. This process results in the multiplication of granulose cells. Preliminary follicles initiate within the foremost week of their subsistence. A differential growth exists in a period of 2 weeks where follicle cells are larger than those before. This is manifested in 3 weeks where the large follicles dominate the ovary. Autoradiography system was first applied by Pedersen in 1972 to conclude the total number of follicles parting the site of non-mounting follicles in a rat at different phases (Sirotkin 2222). This proves that neither a given entity of follicle starts to grow and attains ovulation when the rat matures. Instead, there is always a continuous development growth during infancy (Sirotkin 2222). The wearing of surface ovarian epithelium, which protects ovarian walls, results in the development of ovarian cancer. Entrapped ovarian surface epithelium which covers the ovary contributes to the development of inclusion cysts. The resulting cysts increase the chances of uncontrollable growth of cells probably due to the exposure to the stromal microenvironment which is rich in growth factors. A repeat of such exposure increases the chance of cancer due to the loss of the ovarian basement membrane (Auersperg 246).
During maturity, motion studies indicated that the growth of cycle follicles begins continuously until they fully mature (Pandey and Truica 446). At the final phase (during pregnancy), new follicles began to grow each day. This shows that during the estrous cycle of pregnancy, the number of antral follicles increased significantly. There was also a continuous growth of follicles in rat ovaries during the pregnancy, showing the presence of antral follicles in all phases.
Regulation of ovarian epithelium cells triggers gonadotrophin hormones to stimulate the production of estradiol from follicles. The mitogen estradiol together with other hormones stimulates the proliferation of post-ovulation damaged tissues. Such as luteinizing hormone, play an important role in folliculogenesis. However, if in excess, the hormones trigger the abnormal growth of cells (cancer). The theory behind these observations suggests that exposure to a higher level of hormones at the menopause stage triggers cancer development (Auersperg 246).
Materials and treatments used
Adult rat tissues were used in the experiment. These tissues were subjected to various hormones to learn their morphologies and chemical characteristics. All experimental protocols were observed with respect to recommended animal acts.
Examination results
Multiple pregnancies play a significant role in reducing the chances of ovarian cancer. Recent research shows that breastfeeding and pregnancy reduce the risk of getting cancer. It also hypothesizes that a woman with several numbers of children has a lower risk of contracting cancer as compared to a woman with only one child. Pregnancy is one of the factors which suppress the ovulation process. The ceaseless ovulation hypothesis insinuates that the recurring monthly menstrual sequence of epithelium trauma and successive replacement of worn-out tissues after ovulation triggers apt surroundings for wild mounting of cells. On the other hand, the theory states that ovarian cancer is triggered by an increase in estrogen production and the ovarian surface of proliferation as indicated above (Baby and Bartlewski 19).
FSH and LH levels remained low throughout the pregnancy period except for some instances like in the third week. According to theory, a high level of FSH and LH is known to wear the epithelium, and hence responsible for ovarian cancer. It was found out that there was an interaction between ovary masses and the number of CLs. Progesterone varied throughout the experiment, where maximum values were noted during the mid-pregnancy and then followed by a reduction of the same at the end of pregnancy. On the other hand, estrogen levels during pregnancy were relatively low during the estrous cycle. An increase of apoptotic cells was also noted within the CLs on the third week. Pregnant rats were found to have healthy antral follicles in their ovaries at the beginning of pregnancy, which later disappeared at the mid-period and finally reappeared at the end of pregnancy. OSE had a different structure during pregnancy (Gadducci and Genazzani 108).
Discussion
Various factors modulate intra-ovarian follicles. Epidermal growth factors have a compelling mitogenic repercussion on granulose and theca cells. Hormones regulate the functioning of cells present in the ovary. FSH and LH directly affect theca and granulose cells and are hence fundamental in the growth of follicle cells. At the menopause stage, FSH and LH are released at high levels which increases the risk of uncontrollable cell growth. This is evident when the rat’s estrous cycle is considered. Day three of the pregnancy was associated with an increase in estradiol. This indicates that during the maintenance of follicles large cells take place when their suppression of ovulation occurs. However, it is important to note that the rise of estrogen towards the end of the pregnancy was a result of a decrease in progesterone levels at day 15, and increased activities of follicles cells during development (Modugno, Ness and Cottreau 467).
The rise of estrogen was much lower as compared to the estrogen during the pro-estrus. This is fundamental since it maintains low levels of LH and prolactin, throughout the pregnancy period. Various theories indicate that pregnancy and oral contraceptives reduce ovarian cancer. This is so because ovulation, which is a recurrence of trauma, exposes OSE cells to cancer risks. The risk increases if an individual experiences consecutive ovulation processes. These hypotheses indicate further that breastfeeding also reduces ovarian cancer. This is explained by the fact that pituitary glands, which are involved in the secretion of mammary fluids, alter the concentration of FSH and LH and hence reducing it (Alport et al. 134).
Statistical analysis
Estradiol increases protein biosynthesis which in turn accelerates luteal cell hypertrophy. It also inhibits the prolactin autotrophic mechanism through the impersonation of a synergist. Estradiol indicates synergism to prolactin autotrophic mechanism hence limiting prolactin’s action on the corpus luteum. The increase in the size of rat follicles indicates the importance of FHS and LH in the survival and proliferation of follicle epithelial cells. A respective experiment indicates that apoptosis and atresia of the growing follicles develop as a result of suppression of LHS and LH through hypophysectomy. Treatment of antral follicle cells with hormones upholds apoptosis (Alport et al. 134).
Follicular growth occurs at all ages including even after ovulation has stopped, resulting from the suppression of OSE proliferation, acts antagonistically with endogenous hormone. This enables us to apply this knowledge in the medical treatment of OSE in a primate. Ovarian epithelial is regulated at a high level of gonadotropin, which in turn triggers the secretion of estradiol hormones. Beta estradiol and proliferative response at menopause phase stimulate the rapture of the OSE sites (Azizia and Hardiman 188).
In conclusion, follicular growth has often been termed a continuum. One can establish the difference in follicular growth at an early stage as well as when a follicle is fully developed. Understanding various hormones and their roles in the ovary is very significant in the prevention of ovary-associated diseases, including ovarian cancer. From theories associated with possible causes of cancer, we can conclude that oral contraceptives and recommended number of pregnancies play a significant in the reduction of ovarian cancer risks. Women should also breastfeed as long as they can, to reduce ovarian cancer risk. Understanding that an increased level of androgen can pose a risk during the post-menopause stage is fundamental. This is because necessary precautions can be taken in advance to prevent the risk, by administering oral contraceptives, which can suppress the androgen hormone.
References
Alport, Brie, et al. “Does the Ovarian Stimulation Phase Length Predict In vitro Fertilization Outcomes?” International Journal of Fertility & Sterility 5.3 (2011): 134 – 141. Print.
Auersperg, Nelly. “Ovarian surface epithelium as a source of ovarian cancers: Unwarranted speculation or evidence-based hypothesis?” Gynecologic oncology 130.1 (2013): 246. Print.
Azizia, Mallika, and Paul Hardiman. “Complications of Pregnancy in Women with Polycystic Ovarian Syndrome.” Fetal and Maternal Medicine Review 22.3 (2011): 188 – 206. Print.
Baby, Tanya, and Pawel Bartlewski. “Circulating concentrations of ovarian steroids and follicle-stimulating hormone (FSH) in ewes with 3 or 4 waves of antral follicle emergence per estrous cycle.” Reproductive biology 11.1 (2011): 19. Print.
Gadducci, Angiolo and Andrea Genazzani. “Sex-Steroid Hormones, and Ovarian Carcinogenesis: A Review of Epidemiological and Experimental Data.” Gynecological Endocrinology 18 (2004): 108. Print.
Modugno, Francesmary, Roberta Ness and Carrie Cottreau. “Cigarette Smoking and the Risk of Mucinous and Nonmucinous Epithelial Ovarian Cancer.” Epidemiology 13.4 (2002): 467 – 471. Print.
Pandey, Manjari and Cristina Truica. “Hepatoid carcinoma of the ovary.” Journal of clinical oncology: official journal of the American Society of Clinical Oncology 29.15 (2011): 446. Print.
Sirotkin, Alexander. “Growth factors controlling ovarian functions.” Journal of Cellular Physiology 226.9 (2011): 2222 – 2225. Print.