P F Terranova1, V M Rice. 1. Department of Physiology, University of Kansas Medical Center, Kansas City 66160-7401, USA.
Abstract
PROBLEM: Expression of tumor necrosis factor-alpha (TNF) and interleukins 1 alpha and 1 beta (IL-1) have been reported in ovaries of several species and humans and are implicated in ovarian follicular development and atresia, ovulation, steroidogenesis, and corpus luteum function (including formation, development, and regression). The principal abnormal processes affected by these cytokines are ovarian cancer and reduction of ovarian function during sepsis. METHODS: A literature review. RESULTS: Numerous studies indicate that TNF and IL-1 inhibit gonadotropin-stimulated steroidogenesis of undifferentiated ovarian cells due to inhibition of adenylyl cyclase and post-cAMP sites. In differentiated ovarian cells, these cytokines either stimulate progesterone synthesis or have little to no effect on steroidogenesis. Both cytokines participate in ovulation and levels of these cytokines increase during the preovulatory period. Endotoxin inhibits gonadotropin-stimulated ovarian steroidogenesis and follicular development and these effects are mediated, in part, by TNF and by direct effects of endotoxin on ovarian cells. IN newly formed corpora lutea, progesterone secretion is inhibited by TNF and IL-1, although each has proliferative effects. TNF also has been implicated in regression of corpora lutea because TNF stimulates prostaglandin synthesis and luteal TNF increases after initiation of the decline in progesterone secretion. TNF and IL-1 are secreted by some ovarian cancer cells and stimulate growth of these cells. CONCLUSIONS: Thus, TNF and IL-1 are multifunctional factors affecting various ovarian processes.
PROBLEM: Expression of tumor necrosis factor-alpha (TNF) and interleukins 1 alpha and 1 beta (IL-1) have been reported in ovaries of several species and humans and are implicated in ovarian follicular development and atresia, ovulation, steroidogenesis, and corpus luteum function (including formation, development, and regression). The principal abnormal processes affected by these cytokines are ovarian cancer and reduction of ovarian function during sepsis. METHODS: A literature review. RESULTS: Numerous studies indicate that TNF and IL-1 inhibit gonadotropin-stimulated steroidogenesis of undifferentiated ovarian cells due to inhibition of adenylyl cyclase and post-cAMP sites. In differentiated ovarian cells, these cytokines either stimulate progesterone synthesis or have little to no effect on steroidogenesis. Both cytokines participate in ovulation and levels of these cytokines increase during the preovulatory period. Endotoxin inhibits gonadotropin-stimulated ovarian steroidogenesis and follicular development and these effects are mediated, in part, by TNF and by direct effects of endotoxin on ovarian cells. IN newly formed corpora lutea, progesterone secretion is inhibited by TNF and IL-1, although each has proliferative effects. TNF also has been implicated in regression of corpora lutea because TNF stimulates prostaglandin synthesis and luteal TNF increases after initiation of the decline in progesterone secretion. TNF and IL-1 are secreted by some ovarian cancer cells and stimulate growth of these cells. CONCLUSIONS: Thus, TNF and IL-1 are multifunctional factors affecting various ovarian processes.
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