ROLE OF HORMONAL IMBALANCE IN APOPTOSIS

EFFECT OF HORMONAL IMBALANCE IN APOPTOSIS

Apoptosis is a term used to describe the natural or programmed death of a cell under genetic control. In contrast to necrosis, apoptosis usually does not produce inflammatory reactions in neighboring tissues. There are many endocrine glands in the body; an imbalance of hormone is experienced at different times during life, as the body changes from childhood to adulthood.

            

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Hormonal imbalance occurs as a reaction to the elevated level of estrogen and lowered level of progesterone within a woman’s body and in males many of the unwanted effects of male hormonal imbalance is caused  by  an estrogen dominance. Estrogen is naturally produced by the ovaries and is the female hormone necessary for normal sexual development. Estrogen actions on bones are complex, estrogen effect may be mediated in part by growth factors and interleukin. Osteoclast apoptosis is regulated by estrogen, with estrogen deficiency the Osteoclast live longer and are therefore able to reabsorb more bones. Aromatase inhibitors prevent peripheral estrogen synthesis in post menopausal patients thereby creating estrogen deprivation to stop tumor growth estrogen-induced apoptosis is a plausible molecular mechanism to support an antitumor action physiologic estrogen. Estrogen induced apoptosis in estrogen-deprived ER-positive cell lines in vitro.balance occurs as a reaction to the elevated level of estrogen and lowered level of progesterone within a woman’s body and in males many of the unwanted effects of male hormonal imbalance is caused  by  an estrogen dominance. Estrogen is naturally produced by the ovaries and is the female hormone necessary for normal sexual development. Estrogen actions on bones are complex, estrogen effect may be mediated in part by growth factors and interleukin. Osteoclast apoptosis is regulated by estrogen, with estrogen deficiency the Osteoclast live longer and are therefore able to reabsorb more bones. Aromatase inhibitors prevent peripheral estrogen synthesis in post menopausal patients thereby creating estrogen deprivation to stop tumor growth estrogen-induced apoptosis is a plausible molecular mechanism to support an antitumor action physiologic estrogen. Estrogen induced apoptosis in estrogen-deprived ER-positive cell lines in vitro.

Typically lower fertilization rates are found in women who have polycystic ovaries rather than those with tubal disease or endometriosis. An increased level of estrogen stimulates increased levels of testosterone and androgen (increased body hair). Hyper-androgenism therefore produces layer follicle and increased apoptosis. Mechanism by which androgen induces cyst formation, however excess androgen produces layer follicle and increased apoptosis resulting in cyst formation and follicular atresia(death and regression of an ovarian follicle).

Progesterone is a hormonal balance particularly of estrogen. It enhances beneficial effect of estrogen while mitigating the problems associated with estrogen excess which helps regulate apoptosis. Exogenous estradiol enhances apoptosis in repressing post-partum corpora lutea possibly mediated by prolactin increased level of parathyroid hormone (PTH) stimulates uptake of calcium into the bone and therefore osteoblast apoptosis and deportation of calcium from the bone. PTH also increases the stimulation and secretion of calcitriol. Calcitriol therefore also stimulates osteoblast activity and increases osteoblast apoptosis.

It also has been discovered that rhodamine B increases hypothalamic cell apoptosis and disrupts hormonal balance in rats.  With aging, there is a decline in the level of sex hormone (estrogen, testosterone, dehydroepiandrosterone sulfate) and growth hormone. These particular hormones have great influences on the skin. Balance is critical in the realm of hormones and escalating sex hormones during puberty increases the incidence of skin acne, declining hormonal levels with age accelerates apoptosis of cells in the skin without quick renewal leaching to skin deterioration. Estrogen particularly in menopause is accompanied by significant charges with the skin. Estrogen influence skin thickness, wrinkling and moisture. It binds to receptors on skin cells, activating gene-expression that modulates the skin cell renewal but with declining/low level of estrogen the skin cellular renewal becomes sluggish with regards to rapid rate of cell death (apoptosis). Poorly controlled diabetes is associated with hormonal imbalance including deceased prolactin. In addition to its metabolic action, ghrelin inhibits apoptosis in several cell types. Research in apoptosis shows that between 50-70 billion cells die each day due to apoptosis in average human adult. For an average child between the age of 8 and 14, approximately 20 billion to 30 billion cells die a day. In addition to its importance as a biological phenomenon, defective apoptosis processes have been implicated in an extensive variety of diseases and also to hormonal imbalance. Excessive apoptosis causes atrophy whereas an insufficient amount results from uncontrolled cell proliferation such as cancer. A cell initiates intracellular apoptotic signaling in response to a stress, which may bring about cell suicide. The binding of nuclear receptors by excess glucocorticoids and an increased intracellular calcium concentration, for example by damage to the membrane, can all trigger the release of intracellular apoptotic signals by a damaged cell. A number of cellular such as poly ADP ribose polymerase may also help regulate apoptosis in situations of hormonal imbalance

REFERENCES
Guyton and hall text book of medical physiology 10th edition
Essential of physiology by sembulingam 6th edition
BRS physiology 5th edition, berne and levy physiology

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