Maternal Cocaine Use and Cigarette Smoking in Pregnancy in Relation to Amino Acid Transport and Fetal Growth

Pastrakuljic, Aleksandra; Derewlany, Lidia O.; Koren, Gideon

doi:10.1053/plac.1999.0418

Cited by 98 publications

(50 citation statements)

References 105 publications

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“…Indeed, both structural and functional abnormalities were observed in placentas of humans and rodents exposed to cadmium during pregnancy (9,16,46,74). Proposed mechanisms by which cadmium leads to FGR include reduced uteroplacental blood flow (7, 10, 47) and impaired placental transport function (15,26,49,59). In particular, there is robust evidence that disruption of normal fetoplacental zinc homeostasis is an important mechanism contributing to cadmiuminduced FGR (53).…”

Section: Discussionmentioning

confidence: 99%

Cadmium reduces 11β-hydroxysteroid dehydrogenase type 2 activity and expression in human placental trophoblast cells

Yang¹,

Julan²,

Rubio³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

104

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Section: Discussionmentioning

confidence: 99%

Cadmium reduces 11β-hydroxysteroid dehydrogenase type 2 activity and expression in human placental trophoblast cells

Yang¹,

Julan²,

Rubio³

et al. 2006

American Journal of Physiology-Endocrinology and Metabolism

104

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“…As mentioned, maternal nicotine exposure is known to induce vasoconstriction in placental vasculature, decrease placental blood flow, and reduce trophoblast invasion leading to a delay in the establishment of the fetal-maternal circulation [43] . The subsequent reduction in oxygen supply may cause placental hypoxia, which is also a trigger for further placental modifications including alternations in both the vasculature and uterine wall invasion in order to maintain blood supply to the fetus [44] .…”

Section: Placentationmentioning

confidence: 98%

Smoking-Induced Changes in the Maternal Immune, Endocrine, and Metabolic Pathways and Their Impact on Fetal Growth: A Topical Review

Sabra

Gratacós²,

Roig³

2017

Fetal Diagn Ther

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Perinatal maternal smoking exposure (PMSE) is one of the major environmental risk factors encountered by the fetus. PMSE is usually associated with adverse pregnancy outcomes that may manifest at different stages of life. Nevertheless, fetal growth restriction is the most common smoking-induced side effect. PMSE induces changes in the maternal multiple organ systems. These alterations may affect placentation, which subsequently affects fetal growth. It is worthy to note, however, that the extent of maternal smoking-induced changes depends mainly on the maternal level of susceptibility. Hence, the perinatal pregnancy outcomes vary depending on the interaction between the triad: the maternal, fetal, and placental modifications, making it more complex. In this review, we try to unveil the effect of smoking-induced maternal changes on the maternal immune, endocrine, and metabolic pathways and their impact on fetal growth.

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“…This seems to be the case for cocaine, which readily crosses the placental barrier and enters the fetal circulation. This constitutes a potential cause of adverse effects on the developing fetus in pregnant women consuming this drug [121] . Maternal smoking during pregnancy also decreases the ability of the placenta to efficiently take up amino acids and hence affects the overall transfer of these important metabolites from the maternal to the fetal circulation [121] .…”

Section: Protection Against Drugs and Toxinsmentioning

confidence: 99%

“…Additionally, cocaine may also interact with other placental carriers, such as those involved in monoamine transport [121] . This may affect serotonin and noradrenaline transport across the apical (maternal-facing) plasma membrane of the trophoblast [122] .…”

Section: Protection Against Drugs and Toxinsmentioning

confidence: 99%

Excretion of biliary compounds during intrauterine life

Macı́as¹,

Marin²,

Serrano³

2009

WJG

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In adults, the hepatobiliary system, together with the kidney, constitute the main routes for the elimination of several endogenous and xenobiotic compounds into bile and urine, respectively. However, during intrauterine life the biliary route of excretion for cholephilic compounds, such as bile acids and biliary pigments, is very poor. Although very early in pregnancy the fetal liver produces bile acids, bilirubin and biliverdin, these compounds cannot be efficiently eliminated by the fetal hepatobiliary system, owing to the immaturity of the excretory machinery in the fetal liver. Therefore, the potentially harmful accumulation of cholephilic compounds in the fetus is prevented by their elimination across the placenta. Owing to the presence of detoxifying enzymes and specific transport systems at different locations of the placental barrier, such as the endothelial cells of chorionic vessels and trophoblast cells, this organ plays an important role in the hepatobiliary-like function during intrauterine life. The relevance of this excretory function in normal fetal physiology is evident in situations where high concentrations of biliary compounds are accumulated in the mother. This may result in oxidative stress and apoptosis, mainly in the placenta and fetal liver, which might affect normal fetal development and challenge the fate of the pregnancy. The present article reviews current knowledge of the mechanisms underlying the hepatobiliary function of the fetal-placental unit and the repercussions of several pathological conditions on this tandem.

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Maternal Cocaine Use and Cigarette Smoking in Pregnancy in Relation to Amino Acid Transport and Fetal Growth

Cited by 98 publications

References 105 publications

Cadmium reduces 11β-hydroxysteroid dehydrogenase type 2 activity and expression in human placental trophoblast cells

Cadmium reduces 11β-hydroxysteroid dehydrogenase type 2 activity and expression in human placental trophoblast cells

Smoking-Induced Changes in the Maternal Immune, Endocrine, and Metabolic Pathways and Their Impact on Fetal Growth: A Topical Review

Excretion of biliary compounds during intrauterine life

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