Lipid Peroxidation System in Human Placental Tissue: General Properties and the Influence of Gestational Age

Diamant, Sophia; Kissilevitz, Rita; Diamant, Yoram Z.

doi:10.1095/biolreprod23.4.776

Cited by 37 publications

(30 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MDA is a decomposition product of peroxidized polyunsaturated fatty acids (Mukai & Goldstein 1976). Elevated lipid peroxide levels have also been reported to be greater in third trimester than first trimester human placental tissue (Diamant et al 1980) and are found to be produced by the human placenta during uncomplicated pregnancy (Walsh & Wang 1993).…”

Section: Discussionmentioning

confidence: 99%

Developmental changes in antioxidant enzymatic defences against oxidative stress in sheep placentomes

Garrel¹,

Fowler²,

Al-Gubory³

2010

Journal of Endocrinology

View full text Add to dashboard Cite

Early pregnancy is susceptible to oxidative stress, and thus characterisation of antioxidant systems and pro-and antiapoptotic pathways would improve understanding of placental development and function. We aimed, therefore, to determine the activities of the antioxidant enzymes, copper/zinc-superoxide dismutase (SOD1), manganese-SOD (SOD2), catalase (CAT), glutathione (GSH) peroxidase (GPX) and GSH reductase (GSR); and to quantify the expression of BAX and MCL1 proteins in relation to the developmental changes in antioxidant defences in sheep placentomes sampled on days 35, 55 and 80 of pregnancy. Placentome progesterone content was analyzed to determine steroidogenic capacity. Malondialdehyde (MDA) and protein carbonyl were quantified in placentomes as biomarkers of lipid peroxidation and protein damage respectively. Placentome tissues demonstrated significantly increased content of progesterone and MDA at day 80 of pregnancy and protein carbonyl as early as day 50 of pregnancy. Progesterone and MDA contents were not different between days 35 and 55 of pregnancy. While SOD1 and CAT activities did not alter significantly, SOD2 activity decreased from days 35 to 55. GPX activity increased from days 35 to 55 and increased further to day 80 of pregnancy. GSR activity increased from days 35 to 55 of pregnancy. BAX protein expression decreased, while MCL1 increased from days 35 to 55 and 80 of pregnancy. The increased GPX activity was associated with a decrease in the BAX/MCL1 protein expression ratio. Changes in the antioxidant enzymatic defences could be a part of placentome adaptation to reactive oxygen speciesinduced oxidative stress at specific early developmental stages of pregnancy.

show abstract

Section: Discussionmentioning

confidence: 99%

Developmental changes in antioxidant enzymatic defences against oxidative stress in sheep placentomes

Garrel¹,

Fowler²,

Al-Gubory³

2010

Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…Importantly, OS during the 2 nd trimester of pregnancy is considered a normal occurrence, and is supported by mitochondrial production of lipid peroxides, free radicals, and vitamin E in the placenta that increases as gestation progresses [66-69]. …”

Section: Oxidative Stress In Female Reproductionmentioning

confidence: 99%

The effects of oxidative stress on female reproduction: a review

Agarwal

Aponte-Mellado

Premkumar

et al. 2012

Reprod Biol Endocrinol

1,441

1,188

View full text Add to dashboard Cite

Oxidative stress (OS), a state characterized by an imbalance between pro-oxidant molecules including reactive oxygen and nitrogen species, and antioxidant defenses, has been identified to play a key role in the pathogenesis of subfertility in both males and females. The adverse effects of OS on sperm quality and functions have been well documented. In females, on the other hand, the impact of OS on oocytes and reproductive functions remains unclear. This imbalance between pro-oxidants and antioxidants can lead to a number of reproductive diseases such as endometriosis, polycystic ovary syndrome (PCOS), and unexplained infertility. Pregnancy complications such as spontaneous abortion, recurrent pregnancy loss, and preeclampsia, can also develop in response to OS. Studies have shown that extremes of body weight and lifestyle factors such as cigarette smoking, alcohol use, and recreational drug use can promote excess free radical production, which could affect fertility. Exposures to environmental pollutants are of increasing concern, as they too have been found to trigger oxidative states, possibly contributing to female infertility. This article will review the currently available literature on the roles of reactive species and OS in both normal and abnormal reproductive physiological processes. Antioxidant supplementation may be effective in controlling the production of ROS and continues to be explored as a potential strategy to overcome reproductive disorders associated with infertility. However, investigations conducted to date have been through animal or in vitro studies, which have produced largely conflicting results. The impact of OS on assisted reproductive techniques (ART) will be addressed, in addition to the possible benefits of antioxidant supplementation of ART culture media to increase the likelihood for ART success. Future randomized controlled clinical trials on humans are necessary to elucidate the precise mechanisms through which OS affects female reproductive abilities, and will facilitate further explorations of the possible benefits of antioxidants to treat infertility.

show abstract

“…This oxidation may not be complete; peroxisomes, which perform partial p-oxidation of NEFA [40], have been described in human placental tis sue [11]. In the guinea-pig, experiments in volving the infusion of mixtures of palmitic acids labelled at different positions on the carbon chain, have shown that chain length alterations occur in the placenta, with the release of the shortened NEFA into the fetal compartment [68] (fig.…”

Section: Placental Non-esterified Lipid Transfermentioning

confidence: 99%

Placental Transfer of Non-Esterified Fatty Acids in Normal and Diabetic Pregnancy

Thomas¹

1987

Neonatology

View full text Add to dashboard Cite

The placental transfer of non-esterified fatty acids, predominantly in the direction of mother to fetus, is regulated on a gross scale by the transplacental non-esterified fatty acid gradient. This is maintained by fetal liver lipid uptake and by enhanced lipolysis of circulating triacylglycerol in the pregnant mother. It is also dependent upon maternal placental blood flow, which is reduced in diabetes, upon the fetal umbilical blood flow, upon maternal and fetal albumin concentrations and upon intratrophoblastic fatty acid binding protein, which appears to be altered in diabetes. Circulating maternal tnacylglycerols also directly contribute non-esterified fatty acids to the fetus by intraplacental hydrolysis and the hypertriglyceridaemia associated with maternal diabetes, in concert with changes in lipase levels will enhance maternal to fetal lipid flux.

show abstract

Lipid Peroxidation System in Human Placental Tissue: General Properties and the Influence of Gestational Age

Cited by 37 publications

References 0 publications

Developmental changes in antioxidant enzymatic defences against oxidative stress in sheep placentomes

Developmental changes in antioxidant enzymatic defences against oxidative stress in sheep placentomes

The effects of oxidative stress on female reproduction: a review

Placental Transfer of Non-Esterified Fatty Acids in Normal and Diabetic Pregnancy

Contact Info

Product

Resources

About