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母代孕期和哺乳期尼古丁暴露对 F2 代肺完整性的影响。

The effect of grand maternal nicotine exposure during gestation and lactation on lung integrity of the F2 generation.

机构信息

Department of Medical Biosciences, University of the Western Cape, Bellville, South Africa.

出版信息

Pediatr Pulmonol. 2014 Jan;49(1):67-75. doi: 10.1002/ppul.22783. Epub 2013 Feb 8.

DOI:10.1002/ppul.22783
PMID:23401386
Abstract

BACKGROUND

Maternal nicotine exposure during gestation and lactation adversely affects lung development in the offspring. It has been suggested that the "program" that control long-term maintenance of the structural integrity of the lung may be compromised. The aim of the study was to establish whether the effect of grand-maternal nicotine exposure during gestation and lactation can be transferred to the F2 generation.

METHODS

After mating, rats were randomly divided into two groups (F0). One group received nicotine (1 mg/kg body weight/day). The controls receive saline. Body weight (BW), lung volume (Lv), linear intercept (Lm), alveolar wall thickness (Tsept), senescent and proliferating cell numbers were used to evaluate changes in the lung structure of the offspring (F1). The F1 generation was divided into four groups, namely, (1) control (F1 males mated with F1 females, (2) NmCf (F1 nicotine exposed male mated with F1 control female), (3) NfCm (F1 nicotine exposed female mated with F1 control male), and (4) NmNf (F1 male exposed to nicotine mated with F1 female also exposed to nicotine). The F1 nicotine exposed males and females were exposed to nicotine via the placenta and mother's milk (F0 generation) only. The F2 progeny was never exposed to nicotine.

DISCUSSION

Grand-maternal nicotine (F0) resulted in parenchymal deterioration and emphysema in the F2 progeny due to increased numbers of premature senescent cells together with a slower cell proliferation. The transfer of premature aging characteristics from the F1 progeny to the F2 progeny is via the male and female germ cell line.

CONCLUSION

Grand-maternal nicotine exposure induces structural changes in the lungs of the F2 generation that resembled premature aging.

摘要

背景

母体在妊娠和哺乳期暴露于尼古丁会对后代的肺部发育产生不利影响。有人提出,控制肺结构完整性的长期维持的“程序”可能会受到损害。本研究的目的是确定祖母在妊娠和哺乳期暴露于尼古丁是否会对 F2 代产生影响。

方法

交配后,大鼠被随机分为两组(F0)。一组接受尼古丁(1mg/kg 体重/天)。对照组给予生理盐水。体重(BW)、肺容积(Lv)、线截距(Lm)、肺泡壁厚度(Tsept)、衰老和增殖细胞数量用于评估后代(F1)肺部结构的变化。F1 代分为四组,分别为:(1)对照组(F1 雄性与 F1 雌性交配)、(2)NmCf(F1 尼古丁暴露雄性与 F1 对照雌性交配)、(3)NfCm(F1 尼古丁暴露雌性与 F1 对照雄性交配)和(4)NmNf(F1 雄性暴露于尼古丁并与也暴露于尼古丁的 F1 雌性交配)。F1 尼古丁暴露的雄性和雌性仅通过胎盘和母乳(F0 代)暴露于尼古丁。F2 后代从未接触过尼古丁。

讨论

祖母尼古丁(F0)导致 F2 后代实质恶化和肺气肿,原因是衰老的细胞数量增加,同时细胞增殖较慢。F1 后代向 F2 后代传递过早衰老特征是通过雄性和雌性生殖细胞系。

结论

祖母尼古丁暴露导致 F2 代肺部结构发生类似于早衰的变化。

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