Ann. Pak. Inst. Med. Sci. 2010; 6(2): 91-95

Background: Prenatal Exposure to cigarette smoke has deleterious effects on the placenta and the fetus, which may be due to toxic substances and free radicals present in smoke. The latter cause oxidative injury and therefore, the role of antioxidants need to be investigated as a possible preventive agent.
Objective: To determine, the effects of cigarette smoke on maternal fetal barrier and to observe the preventive role of antioxidants if any.
Materials and Methods: 51 female mice (Balb C strain) were mated and grouped: Groups C: control, S: exposed to smoke and SV: exposed to smoke and given antioxidants (vitamin C, E) and sacrificed at 19 dpc (days post coitus). 14 animals from C, 12 from S and 14 from SV had healthy pregnancies. Their placentae were studied microscopically. The thickness of the maternal fetal barrier and the distance between mononuclear trophoblast cells in the maternal sinusoids were measured.
Results: The thickness of maternal fetal barrier, and the distance between mononuclear trophoblast cells in the S group (2.21±1.35μm, 38.36±2.05μm) were significantly greater than in the Control (1.31±0.04μm, 33.48±1.00μm) with P=0.0001 and P=0.01 respectively. The thickness of the barrier in the SV (1.66±0.09μm) was significantly thinner than the S group (P=0.002).The distance between mononuclear trophoblast cells in the SV did not increase significantly (33.58±1.37μm: P=0.17) as compared to the Control.
Conclusion: Cigarette smoke causes thickening of the maternal fetal barrier which could be ameliorated significantly by antioxidants. Therefore, these effects may be partly due to oxidative injury produced by free radicals present in the smoke.
Key Words:Cigarette smoke. Free radicals. Antioxidants


Introduction

Cigarette smoking is an international problem and according to an estimate by WHO, if the present smoking patterns continue, smoking is expected to be responsible for death of 10 million people every year by 2020.¹ Cigarette smoke contains many toxic chemicals², and a high concentration of free radicals which may cause oxidative injury in the body.³ It is associated with oxidative stress leading to an up regulation of antioxidant systems; which in turn help in reducing the oxidative load.⁴ Cigarette smoke harms nearly all systems of the body reducing quality of life and life expectancy. As fetuses have immature systems and their antioxidant enzymatic processes are not fully developed, therefore if exposed to smoke (through the placenta) in utero, they form a vulnerable population for adverse effects.⁵ Since placenta is a maternofetal organ which is needed for the exchange of gases, nutrients and waste products between the mother and fetus, any environmental insult that affects the placenta can lead to placental insufficiency, fetal growth retardation and even death.⁶ Therefore prenatal exposure to cigarette smoke, along with other injurious effects, has also been linked with low birth weight and increased perinatal mortality.⁷
Studies regarding the effects of cigarette smoke on the morphology of human placenta have shown a number of histological changes linked with tobacco exposure. These include an increase in thickness of subtrophoblastic membrane8 and hyperplasia of cytotrophoblast cells.⁹ These observations relate with an impaired exchange of gases and nutrients between the mother and fetus, thereby increasing the risk of under nourishment of the fetus.¹⁰ Similar studies on mice have also shown adverse effects of cigarette smoke on mouse placenta.¹¹
The laboratory mouse belongs to the order Rodentia and is a good example of the placentalia. In mice, the main placenta is chorioallontoic, which is made up of a single cotyledon which is discoid. Three regions can be distinctly identified in the placenta from without inwards.
1. Giant cell layer: They are homologous to the extravillous cytotrophoblast cells in the humans, and are responsible for accomplishing implantation.¹⁰
2. Spongiotrophoblast layer: These cells are homologous to the cytotrophoblast cell columns in the primates.¹²
3. Labyrinthine Layer: This layer constitutes the major site of maternal fetal exchange. The barrier between the maternal and fetal blood being hemochorial6. It is homologous to the chorionic villi in the primates. The trophoblast cells with their associated fetal vessels and maternal channels create this densely packed layer. The chorionic trophoblast cells differentiate to create a trilaminar epithelium.
• A layer of mononuclear trophoblast cells lying adjacent to the maternal vascular channel.
• An intermediate layer of syncytiotrophoblast cells.
• Another layer of syncytiotrophoblast cells which is in direct apposition to the endothelial cells of the fetal derived blood vessels and separated from them only by the basement membrane. ⁶
Although experimental studies are available regarding the beneficial effects of antioxidants in neutralizing some of the harmful effects of tobacco smoke, however direct histological study of placenta and the extent of the preventive effects produced by antioxidant has not been carried out. Keeping this in mind an experimental study was planned using the laboratory mice. The objective of the study was to observe the effects of cigarette smoke on histology of mouse placenta especially the thickness of the maternal fetal barrier and to observe the role of antioxidants in preventing those changes.