Abstract
Identification of a new agent from natural products for the protection of embryonic anomalies is potentially valuable. To investigate the protective effect exerted by lycopene against nicotine-induced malformations, mouse embryos in embryonic day 8.5 with yolk sac placentas were cocultured with 1 mM nicotine and/or lycopene (1 × 10−6, 1 × 10−5 μM) for 48 h. The morphological defects and apoptotic cell deaths in the embryo and yolk sac placenta of the nicotine group were significantly increased. Exposure to nicotine resulted in reduced superoxide dismutase (SOD) activity and cytoplasmic SOD and cytoplasmic glutathione peroxidase mRNA levels, but increased lipid peroxidation level in embryos. Moreover, treatment with nicotine resulted in aggravated expressions of the mRNA or protein level of antiapoptotic (BCL2-associated X protein, B-cell lymphoma-extralarge, and caspase 3), anti-inflammatory (nuclear factor kappa-light-chain-enhancer of activated B cells and tumor necrosis factor-alpha), and vasculogenic (vascular endothelial growth factor-alpha, insulin-like growth factor-1, alpha smooth muscle actin, transforming growth factor-beta 1, and hypoxia inducible factor-1 alpha) factors in the embryo and yolk sac placenta. However, all the parameters were significantly improved by treatment with lycopene, as compared to the nicotine group. These findings indicate the potential of lycopene as a protective agent against embryonic anomalies and yolk sac vasculogenic and placenta-forming defects induced by nicotine through modulations of oxidative, apoptotic, vasculogenic, and inflammatory activities.
Highlights
Maternal smoking during early pregnancy has undesirable effects on the fetal organs and tissue development [1]
Morphological scores altered by nicotine treatment were significantly inhibited in embryos cotreated with lycopene (Tables 2 and 3, Figure 1; P < 0:05)
Embryos treated with nicotine showed growth retardation, pale color, immature organization, and abnormal yolk sac morphology with marked reduction in size, impaired vascular branching, and a ring of blood islands around the Primer vascular endothelial growth factor (VEGF)-α
Summary
Maternal smoking during early pregnancy has undesirable effects on the fetal organs and tissue development [1]. The adverse effects of maternal smoking on embryonic development lead to low birth weight, premature labor, stillbirth, birth defects, and congenital malformations in the offspring [2]. A major toxic component among the thousands of substances present in cigarettes, is regarded as the causative agent of fetal anomalies [3]. Nicotine induces ROS (reactive oxygen species), resulting in damage to the embryonic cells [7]. It is necessary to research the effects of smoking-induced malformation and identify natural preventive substances that can be consumed during pregnancy
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