小鼠围产期暴露于二氧化钛纳米粒子后代呼吸缺陷的多代遗传。

0 MATERIALS SCIENCE, MULTIDISCIPLINARY
Marie Boulain, Didier Morin, Laurent Juvin
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引用次数: 0

摘要

背景:近几十年来,二氧化钛纳米粒子(TIO2NPs)的使用量大幅增加,目前在各种日常消费品中都能常见到这种粒子。由于尺寸较小,TIO2NPs 可以穿透生物屏障,与生物组织产生不良相互作用。值得注意的是,孕妇在围产期接触 TIO2NPs 已被证明会干扰后代的生长。此外,这种接触还会诱导新生儿的 DNA 发生表观遗传学改变,从而可能产生多代效应。因此,围产期暴露于 TIO2NPs 可能会立即诱发新生儿代谢障碍,并可能长期遗传给后代:在这项研究中,我们利用雌性小鼠围产期自愿摄入食物的方式暴露于 TIO2NPs,观察到新生雌雄 F1 后代的代谢受损情况。与未暴露的动物相比,暴露的新生小鼠体重增加减少,呼吸频率减慢。此外,暴露的 F1 新生小鼠出现呼吸暂停的比例较高。当暴露仅限于产后期间时,也会出现类似的观察结果,这表明哺乳期是 TIO2NPs 对产后代谢产生不利影响的关键时期。重要的是,TIO2NPs 诱导的呼吸障碍会从 F1 雌性传给随后的 F2 后代。此外,成年 F1 雌性再次暴露于 TIO2NPs 会加剧新生 F2 雄性的呼吸障碍:我们的研究结果表明,围产期暴露于 TIO2NPs 会干扰后代的体重增加和呼吸,而且这些缺陷会遗传给后代。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Multigenerational inheritance of breathing deficits following perinatal exposure to titanium dioxide nanoparticles in the offspring of mice.

Multigenerational inheritance of breathing deficits following perinatal exposure to titanium dioxide nanoparticles in the offspring of mice.

Background: The utilization of titanium dioxide nanoparticles (TIO2NPs) has experienced a significant surge in recent decades, and these particles are now commonly found in various everyday consumer products. Due to their small size, TIO2NPs can penetrate biological barriers and elicit adverse interactions with biological tissues. Notably, exposure of pregnant females to TIO2NPs during the perinatal period has been shown to disrupt the growth of offspring. Furthermore, this exposure induces epigenetic modifications in the DNA of newborns, suggesting the possibility of multigenerational effects. Thus, perinatal exposure to TIO2NPs may induce immediate metabolic impairments in neonates, which could be transmitted to subsequent generations in the long term.

Results: In this study, we utilized perinatal exposure of female mice to TIO2NPs through voluntary food intake and observed impaired metabolism in newborn male and female F1 offspring. The exposed newborn mice exhibited reduced body weight gain and a slower breathing rate compared to non-exposed animals. Additionally, a higher proportion of exposed F1 newborns experienced apneas. Similar observations were made when the exposure was limited to the postnatal period, highlighting lactation as a critical period for the adverse effects of TIO2NPs on postnatal metabolism. Importantly, the breathing deficits induced by TIO2NPs were transmitted from F1 females to the subsequent F2 generation. Moreover, re-exposure of adult F1 females to TIO2NPs exacerbated the breathing deficits in newborn F2 males.

Conclusions: Our findings demonstrate that perinatal exposure to TIO2NPs disrupts postnatal body weight gain and respiration in the offspring, and these deficits are transmissible to future generations.

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