METABOLISM OF POLYNUCLEAR AROMATIC HYDROCARBON IN HUMAN TERM PLACENTAINFLUENCED BY CIGARETTE-SMOKE EXPOSURE

Citation
Mk. Sanyal et al., METABOLISM OF POLYNUCLEAR AROMATIC HYDROCARBON IN HUMAN TERM PLACENTAINFLUENCED BY CIGARETTE-SMOKE EXPOSURE, Reproductive toxicology, 8(5), 1994, pp. 411-418
Citations number
45
Categorie Soggetti
Reproductive Biology",Toxicology
Journal title
ISSN journal
08906238
Volume
8
Issue
5
Year of publication
1994
Pages
411 - 418
Database
ISI
SICI code
0890-6238(1994)8:5<411:MOPAHI>2.0.ZU;2-5
Abstract
The relative contributions of biologic and environmental factors on em bryo-fetal development were elucidated in a population of pregnant wom en who were exposed to varying amounts of active cigarette smoke and w omen who were not exposed to cigarette smoke. The neonatal weight at b irth, placental weight at delivery, duration of pregnancy, and placent al xenobiotic (polynuclear aromatic hydrocarbon, PAH) metabolism poten tial were assessed in this population. The overall metabolic capabilit y in exposed and unexposed placental tissue was measured by in vitro a ssays using microsomes and a PAH substrate, benzo[a]pyrene (B[a]P). To xicity potential was determined by B[a]P-metabolite-DNA adduct generat ion under the same incubation condition. Cigarette smoke exposure incr eased the overall PAH metabolism potential in placental tissues by app roximately 200% (nonsmoker 176.2 +/- 33.6, n = 25; smoker 524.5 +/- 75 .5, n = 32 pmol/mg protein) whereas PAH-DNA adduct formation potential did not increase significantly over the basal level (nonsmoker 5002 /- 830, n = 15; smoker 6172 +/- 1443, n = 22 fmol B[a]P equivalent/mu mol DNA/mg protein). Exposure to cigarette smoke during pregnancy is d eleterious to fetal development as reflected by reduced neonatal weigh t at birth. In contrast, placental weight reduction is indistinct, but placentae expressed markedly augmented overall xenobiotic (PAH) metab olism capability in response to cigarette smoke exposure during pregna ncy, indicating placental metabolism may be an important mediator of a dverse effects induced by such xenobiotic exposure.