The fundamental role of increased production of nitric oxide in lipopolysaccharide-induced embryonic resorption in mice

Ogando, D.; Paz, Dante A.; Cella, Maximiliano; Franchi, A

doi:10.1530/rep.0.1250095

Cited by 97 publications

(58 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…LPS has been associated with adverse pregnant outcomes in rodent animals. According to an earlier report, mice exposed to LPS at early gestational stage caused embryonic resorption [3]. We and others showed that mice exposed to LPS at late gestational stage resulted in fetal demise, intra-uterine growth restriction (IUGR), skeletal development retardation, and preterm delivery [4]–[8].…”

Section: Introductionmentioning

confidence: 97%

Orally Administered Melatonin Prevents Lipopolysaccharide-Induced Neural Tube Defects in Mice

Chen

et al. 2014

PLoS ONE

View full text Add to dashboard Cite

Lipopolysaccharide (LPS) has been associated with adverse pregnant outcomes, including fetal demise, intra-uterine growth restriction (IUGR), neural tube defects (NTDs) and preterm delivery in rodent animals. Previous studies demonstrated that melatonin protected against LPS-induced fetal demise, IUGR and preterm delivery. The aim of the present study was to investigate the effects of melatonin on LPS-induced NTDs. All pregnant mice except controls were intraperitoneally injected with LPS (25 µg/kg) daily from gestational day (GD)8 to GD12. Some pregnant mice were orally administered with melatonin (MT, 50 mg/kg) before each LPS injection. A five-day LPS injection resulted in 27.5% of fetuses with anencephaly, exencephaly or encephalomeningocele. Additional experiment showed that maternal LPS exposure significantly down-regulated placental proton-coupled folate transporter (pcft) and disturbed folate transport from maternal circulation through the placentas into the fetus. Interestingly, melatonin significantly attenuated LPS-induced down-regulation of placental pcft. Moreover, melatonin markedly improved the transport of folate from maternal circulation through the placentas into the fetus. Correspondingly, orally administered melatonin reduced the incidence of LPS-induced anencephaly, exencephaly or encephalomeningocele. Taken together, these results suggest that orally administered melatonin prevents LPS-induced NTDs through alleviating LPS-induced disturbance of folate transport from maternal circulation through the placenta into the fetus.

show abstract

Section: Introductionmentioning

confidence: 97%

Orally Administered Melatonin Prevents Lipopolysaccharide-Induced Neural Tube Defects in Mice

Chen

et al. 2014

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…In human, Gram-negative bacterial infections are recognized as a cause of fetal loss and preterm labor [4], [5]. Mimicking maternal infection by exposing the pregnant rodents to LPS during the first trimester resulted in embryonic resorption and fetal death [6], [7]. Maternal LPS exposure during the second trimester caused fetal death and preterm delivery [8].…”

Section: Introductionmentioning

confidence: 99%

Maternal LPS Exposure during Pregnancy Impairs Testicular Development, Steroidogenesis and Spermatogenesis in Male Offspring

Wang

Yang

et al. 2014

PLoS ONE

View full text Add to dashboard Cite

Lipopolysaccharide (LPS) is associated with adverse developmental outcomes including embryonic resorption, fetal death, congenital teratogenesis and fetal growth retardation. Here, we explored the effects of maternal LPS exposure during pregnancy on testicular development, steroidogenesis and spermatogenesis in male offspring. The pregnant mice were intraperitoneally injected with LPS (50 µg/kg) daily from gestational day (GD) 13 to GD 17. At fetal period, a significant decrease in body weight and abnormal Leydig cell aggregations were observed in males whose mothers were exposed to LPS during pregnancy. At postnatal day (PND) 26, anogenital distance (AGD), a sensitive index of altered androgen action, was markedly reduced in male pups whose mothers were exposed to LPS daily from GD13 to GD 17. At PND35, the weight of testes, prostates and seminal vesicles, and serum testosterone (T) level were significantly decreased in LPS-treated male pups. At adulthood, the number of sperm was significantly decreased in male offspring whose mothers were exposed to LPS on GD 13–17. Maternal LPS exposure during gestation obviously diminished the percent of seminiferous tubules in stages I–VI, increased the percent of seminiferous tubules in stages IX–XII, and caused massive sloughing of germ cells in seminiferous tubules in mouse testes. Moreover, maternal LPS exposure significantly reduced serum T level in male mice whose mothers were exposed to LPS challenge during pregnancy. Taken together, these results suggest that maternal LPS exposure during pregnancy disrupts T production. The decreased T synthesis might be associated with LPS-induced impairments for spermatogenesis in male offspring.

show abstract

“…Nitric oxide (NO) plays important roles during pregnancy in implantation, decidualisation, vasodilatation of decidual, placental and uterine vessels and myometrial relaxation (Sladek et al 1997;Chwalisz et al 1999;Chwalisz and Garfield 2000;Ogando et al 2003). It has also been reported that NO participates in vascular invasion of the trophoblast (Ariel et al 1998) and infection control during pregnancy (Nowicki et al 1997).…”

Section: Introductionmentioning

confidence: 99%

Metformin prevents embryonic resorption induced by hyperandrogenisation with dehydroepiandrosterone in mice

Solano¹,

Elia²,

Luchetti³

et al. 2006

Reprod. Fertil. Dev.

View full text Add to dashboard Cite

The present study examined the mechanism by which metformin prevents dehydroepiandrosterone (DHEA)-induced embryonic resorption in mice. Treatment with DHEA (6 mg/100 g bodyweight, 24 and 48 h post implantation) induced 88 +/- 1 % embryonic resorption and the diminution of both serum oestradiol (E) and progesterone (P) levels. However, when metformin (50 mg/kg bodyweight) was given together with DHEA, embryo resorption (43 +/- 3% v. 35 +/- 5% in controls) and both serum E and P levels were not significantly different from controls. Glucose and insulin levels were increased in the DHEA-treated mice but when metformin was administered together with DHEA these parameters were similar to control values. Treatment with DHEA increased ovarian oxidative stress and diminished uterine nitric oxide synthase (NOS) activity; however, when metformin was administered together with DHEA, both ovarian oxidative stress and uterine NOS activity were not different from controls. Metformin treatment did not modify the percentage of CD4(+) and CD8(+) T cells from both axillar and retroperitoneal lymph nodes but prevented the increase of serum tumour necrosis factor +/- produced in DHEA-treated mice. These results show that metformin acts in DHEA-induced embryonic resorption in mice by modulating endocrine parameters, ovarian oxidative stress and uterine NOS activity.

show abstract

The fundamental role of increased production of nitric oxide in lipopolysaccharide-induced embryonic resorption in mice

Cited by 97 publications

References 22 publications

Orally Administered Melatonin Prevents Lipopolysaccharide-Induced Neural Tube Defects in Mice

Orally Administered Melatonin Prevents Lipopolysaccharide-Induced Neural Tube Defects in Mice

Maternal LPS Exposure during Pregnancy Impairs Testicular Development, Steroidogenesis and Spermatogenesis in Male Offspring

Metformin prevents embryonic resorption induced by hyperandrogenisation with dehydroepiandrosterone in mice

Contact Info

Product

Resources

About