Oxygen Radicals and Reactive Oxygen Species in Reproduction

Riley, John C. M.; Behrman, Harold R.

doi:10.3181/00379727-198-43321c

Cited by 165 publications

(74 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…consistent with previous findings about the role of PGF 2a in the generation of ROS and the luteotrophic role of PGE (Riley & Behrman 1991, Sawada & Carlson 1991, Motta et al 2001a, Minegishi et al 2002. Metformin treatment prevented the effects of DHEA since neither LPO (Fig.…”

Section: Dhea and Metformin In CLsupporting

confidence: 81%

Effect of DHEA and metformin on corpus luteum in mice

Sander¹,

Facorro²,

Piehl³

et al. 2009

Reproduction

View full text Add to dashboard Cite

We evaluated the effect of hyperandrogenism in ovaries with functional and regressing corpora lutea (CL) and the action of metformin in preventing these possible alterations using a mouse model. To obtain a CL functional for 9G1 days, immature female mice of the BALB/c strain were injected i.p. with 10 IU/mouse of pregnant mare's serum gonadotropin (PMSG). DHEA (60 mg/kg body weight s.c., 24 and 48 h prior to kill) decreased both serum progesterone (P) and estradiol (E 2 ) levels and increased the activity of superoxide dismutase (SOD) from ovaries with functional CL (on day 5 after PMSG). It increased P and E 2 and the activities of SOD and catalase (CAT) and decreased lipoperoxidation of ovaries with regressing CL (on day 9 after PMSG). Treatment with DHEA did not affect the production of prostaglandin F 2a (PGF 2a ) or PGE by ovaries with functional CL, whereas DHEA decreased PGF 2a and increased PGE production by ovaries with regressing CL. Metformin (50 mg/kg body weight, orally) given together with DHEA restored E 2 levels from mice with ovaries with functional CL and serum P, PGF 2a and PGE levels, and oxidative balance in mice with ovaries with regressing CL. Metformin alone was able to modulate serum P and E 2 levels, lipoperoxidation, SOD and CAT, and the 5,5-dimethyl-1-pyrroline N-oxide/ % OH signal. These findings suggest that hyperandrogenism is able to induce or to rescue CL from luteolysis and metformin treatment is able to prevent these effects.

show abstract

Section: Dhea and Metformin In CLsupporting

confidence: 81%

Effect of DHEA and metformin on corpus luteum in mice

Sander¹,

Facorro²,

Piehl³

et al. 2009

Reproduction

View full text Add to dashboard Cite

show abstract

“…More marked inhibition of ovulation by NDGA might be ascribed to two additional effects of this inhibitor. One is an antioxidant property (Carlson et al 1995, Takami et al 1999 since oxidative stress contributes to the ovulation process (Riley & Behrman 1991), and another is some cross-reactivity with COX that becomes expressed at the high dose (Van Wauwe & Goossens 1983, Miyazawa et al 1985. Preovulatory follicles that looked healthy and were with the largest diameter over 500 mm were examined for indicated numbers of ovaries in each group.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of ovulation by a lipoxygenase inhibitor involves reduced cyclooxygenase-2 expression and prostaglandin E2 production in gonadotropin-primed immature rats

Kurusu¹,

Jinno²,

Ehara³

et al. 2009

Reproduction

View full text Add to dashboard Cite

Potential roles of cyclooxygenase (COX) pathway of arachidonic acid (AA) metabolism are established in a murine model of induced ovulation. Pharmacological inhibition of an alternative lipoxygenase (LOX) pathway has been shown to cause defective ovulation, but the mechanism is still undefined. This study investigated the effects of two LOX inhibitors and their time dependency on ovulation and COX activity in gonadotropins (eCG and human chorionic gonadotropin (hCG))-primed immature rats. Intra-ovarian bursal treatment with a general LOX inhibitor nordihydroguaiaretic acid (NDGA) at 0 h post-hCG (hCG0h) dose dependently inhibited ovulation rate. The drug was still but less effective when treated at hCG6h. A more specific inhibitor, 3,4-dihydroxyphenyl ethanol (DPE) was also inhibitory when treated at hCG0h but not at hCG6h. Interestingly, treatment with DPE at hCG0h resulted in attenuated expression of immunoreactive PTGS2 in granulosa layers and concomitant decrease in ovarian prostaglandin E 2 (PGE 2 ) content at hCG8h. NDGA treatment reduced immunoreactive PTGS2. Ovulatory impairment by both inhibitors was prevented by systemic administration of PGE 2 at hCG6h. Immunohistochemistry revealed the expression of ALOX5 and ALOX12 in both thecal and granulosa layers of preovulatory follicles and, notably, the augmented immunoreactivities during 8 h after hCG treatment. Our results indicate the probable presence of multiple LOX isoforms and that specific inhibition of LOX at an early stage of hCG-signaling led to reduced PTGS2 activity and thus defective ovulation. They reveal a probable relationship between two pathways of AA metabolism and account at least partly for the mechanism by which the LOX inhibitor causes impaired ovulation.

show abstract

“…Reactive oxygen species may be released in connection with follicle rupture, because inhibition of oxygen free radicals leads to inhibition of ovulation (17). Reactive oxygen species are thought to play a role in oocyte maturation (18). Polychlorinated biphenyls (19, 20) and hexachlorobenzene (21), both notorious xenobiotics, have been demonstrated in the FF of patients undergoing IVF and are known to induce glutathione S-transferases in tissues other than the ovaries (22, 23).…”

Section: Follicular Glutathione S-transferasementioning

confidence: 99%