Endogenous levels of prostaglandin F2α and its main metabolites in plasma and endometrium of normal and dysmenorrheic women

Lundström, V.; Green, K.

doi:10.1016/0002-9378(78)90320-4

Cited by 207 publications

(82 citation statements)

References 12 publications

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“…Dysmenorrhoea is associated with uterine hypercontractility resulting in episodes of reduced endometrial blood flow leading to ischaemia and increased pain (Rees 1989). This observation may be a consequence of increased PGF 2a production as explants from women with dysmenorrhoea produce more PGF 2a in response to arachidonic acid compared with normal endometrial explants (Lundstrom & Green 1978). Further evidence of the role of PGs comes from the administration of COX enzyme inhibitors such as ibuprofen, which have been demonstrated to reduce menstrual blood flow (Makarainen & Ylikorkala 1986) and selective COX2 inhibitors that have been used in the treatment of dysmenorrhoea and heavy menstrual blood loss (Daniels et al 2002).…”

Section: Menstrual Disordersmentioning

confidence: 99%

Inflammatory pathways in female reproductive health and disease

Jabbour¹,

Sales²,

Catalano³

et al. 2009

Reproduction

291

226

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Inflammation involves alterations to vascular and immune cell function. It is well recognised that many physiological reproductive events such as ovulation, menstruation, implantation and onset of labour display hallmark signs of inflammation. These are orchestrated by specific molecular pathways involving a host of growth factors, cytokines, chemokines and lipid mediators. Resumption of normal reproductive function involves prompt and proper resolution of these inflammatory pathways. Recent literature confirms that resolution of inflammatory pathways involves specific biochemical events that are activated to re-establish homeostasis in the affected tissue. Moreover, initiation and maintenance of inflammatory pathways are the key components of many pathologies of the reproductive tract and elsewhere in the body. The onset of reproductive disorders or disease may be the result of exacerbated activation and maintenance of inflammatory pathways or their dysregulated resolution. This review will address the role of inflammatory events in normal reproductive function and its pathologies.

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Section: Menstrual Disordersmentioning

confidence: 99%

Inflammatory pathways in female reproductive health and disease

Jabbour¹,

Sales²,

Catalano³

et al. 2009

Reproduction

291

226

View full text Add to dashboard Cite

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“…In addition, PGE 2 and PGF 2α concentrations are higher in the menstrual fluid of women with dysmenorrhoea than in women with painless periods (Rees et al, 1984b;Rees, 1989). Studies in vitro have demonstrated that endometrial explants from women with dysmenorrhoea produce more PGF 2α in response to arachidonic acid compared with endometrium from pain-free women (Lundstrom and Green, 1978). This finding has prompted the use of COX enzyme inhibitors such as mefenamic acid, ibuprofen and naproxen as therapeutic regimens for management of this disorder; treatment being administered during menstruation, or before the onset of menses (Rees, 1989).…”

Section: Dysmenorrhoeamentioning

confidence: 99%

Cyclooxygenase enzymes and prostaglandins in pathology of the endometrium

Sales¹

2003

Reproduction

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Prostaglandins are bioactive lipids produced from arachidonic acid by cyclooxygenase (COX) enzymes and specific terminal prostanoid synthase enzymes. After biosynthesis, prostaglandins exert an autocrine-paracrine function by coupling to specific prostanoid G protein-coupled receptors to activate intracellular signalling and gene transcription. For many years, prostaglandins have been recognized as key molecules in reproductive biology by regulating ovulation, endometrial physiology and proliferation of endometrial glands and menstruation. More recently, a role for COX enzymes and prostaglandins has been ascertained in reproductive tract pathology, including carcinomas, menorrhagia, dysmenorrhoea and endometriosis. Although the mechanism by which prostaglandins modulate these pathologies is still unclear, a large body of evidence supports a role for COX enzymes, prostaglandins and prostaglandin receptor signalling pathways in angiogenesis, apoptosis and proliferation, tissue invasion and metastases and immunosuppression. Here, an overview is provided of some of the findings from these studies with specific emphasis on the role of COX enzymes, prostaglandin E 2 and F 2α in disorders of endometrial proliferation and menstruation in non-pregnant women.The arachidonic acid cascade generates a family of bioactive lipids, including prostaglandins, thromboxanes and leukotrienes that modulate diverse physiological and pathophysiological responses in the reproductive tract. There has been a great deal of interest over the past few years in the involvement of arachidonic acid metabolites in pathology. However, there is still much uncertainty about the manner in which they contribute to specific phenotypic cellular changes that may precipitate pathophysiology. The focus of this review is to provide some insight into the role of cyclooxygenase (COX) enzymes, prostaglandin E 2 (PGE 2 ) and PGF 2α and their respective receptors in reproductive pathophysiology, with specific regard to disorders of endometrial proliferation and dysfunctional menstruation.The kinetics of the prostaglandin biosynthetic pathway is driven by the availability of free arachidonic acid. When released from plasma membrane phospholipids or dietary fatty acids, after activation of phospholipase A2 (PLA2) or PLC, arachidonic acid is cyclized and oxygenated by COX enzymes by addition of the 15-hydroperoxy group to form prostaglandin G 2 (PGG 2 ). The hydroperoxy group of PGG 2 is reduced to the hydroxy group of PGH 2 (Marnett, 1992) (Fig. 1). This intermediate serves as the substrate for terminal prostanoid synthase enzymes. These enzymes are named according to the prostaglandin they produce, such that prostaglandin D 2 is synthesized by prostaglandin-D-synthase (PGDS), prostaglandin E 2 (PGE 2 ) by prostaglandin-E-synthase (PGES); prostaglandin F 2α by

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“…Primary dysmenorrhea is derived from an abnormal increase in the contractile activity of the uterus [41]. It is usually due to functional immaturity in ovarian sex steroid hormone production that stimulates local production of chemical mediators such as prostaglandins E2, F2 and leukotrienes in the uterus during menstruation [42]. Clinically, when the matured women have dysmenorrhea without apparent signs for ovarian dysfunction such as irregular menstruation, several organic disorders such as uterine myoma should be suspected.…”

Section: B Dysmenorrheamentioning

confidence: 99%

“…Dysmenorrhea is an important sign of functional disturbance in the hypothalamic-pituitary-ovarian axis and subsequent local inflammation in the pelvic cavity [39][40][41][42][43], which also is an excellent parameter that reflects female psychophysiological status. It begins within 6-12 months from the menarche and is characterized by localized pain in the abdominal inferior quadrants.…”

Section: B Dysmenorrheamentioning

confidence: 99%

Adverse Effects of Dietary Habits on Menstrual Disorders in Young Women

Fujiwara¹,

Sato²,

Awaji³

et al. 2007

TOFSJ

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It has been accepted that food customs are closely associated with quality of life in women of the reproductive age. Food customs are speculated to not only influence the present life style but also to induce gynecological disorders such as dysmenorrhea and irregular menstruation. Although there is no constant definition of regular or normal menstruation, epidemiologic evaluation of menstrual cycle has been becoming an important issue. In addition, latent development of organic diseases such as endometriosis, which are accompanied by dysmenorrhea, is a concern under the current nutritional environment in young women. Thus, it is an important issue to evaluate the present situation of eating habits in young women and estimate the influence of these habits on the quality of reproductive functions. Therefore, in this review, recent articles that are concerned with these issues have been reevaluated.

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Endogenous levels of prostaglandin F2α and its main metabolites in plasma and endometrium of normal and dysmenorrheic women

Cited by 207 publications

References 12 publications

Inflammatory pathways in female reproductive health and disease

Inflammatory pathways in female reproductive health and disease

Cyclooxygenase enzymes and prostaglandins in pathology of the endometrium

Adverse Effects of Dietary Habits on Menstrual Disorders in Young Women

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