小鼠大脑色氨酸/犬尿氨酸和谷氨酸系统对青少年暴露于高浓度环境超细粒子空气污染的易感性具有雄性特征

IF 3.4 3区 医学 Q2 NEUROSCIENCES Neurotoxicology Pub Date : 2024-07-11 DOI:10.1016/j.neuro.2024.07.004
D.A. Cory-Slechta , E. Marvin , K. Welle , C. Goeke , D. Chalupa , G. Oberdörster , M. Sobolewski
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引用次数: 0

摘要

空气污染(AP)暴露与许多神经发育和精神疾病有关,包括自闭症谱系障碍、注意缺陷多动障碍和精神分裂症,所有这些疾病都偏向男性,发病期从生命早期到青春期晚期/成年早期。以前的实验研究主要关注大脑早期发育过程中接触杀伤性物质的影响,但实际上大脑发育一直延续到成年早期。目前在小鼠身上进行的研究试图扩展人们对青春期大脑发育脆弱性的认识,青春期是大脑发育和成熟的晚期,但对被认为是反应性最强的 AP 的超细微粒(UFPs)成分具有重要影响。此外,它还研究了青少年在早期发育暴露之前对超细微粒的反应,以确定影响的轨迹和潜在的增强或减轻不良后果。研究结果侧重于与多种神经发育障碍相关的共同特征。为此,C57Bl/6J雌雄小鼠在出生后第4-7天和第10-13天暴露于高浓度UFP或过滤空气中,并在出生后第39-42天和第45-49天再次暴露于高浓度UFP或过滤空气中,结果每种性别有3个暴露于出生后/青少年处理组:空气/空气组、空气/UFP组和UFP/UFP组。在 PND50 时检查神经发育障碍的常见特征。产后接触的总浓度平均为 44.34 μg/m3 ,青少年接触的总浓度平均为 49.18 μg/m3。男性大脑在青春期特别容易受到 UFP 暴露的影响,额叶皮层和纹状体谷氨酸能神经递质和色氨酸/羟色胺能神经递质会发生改变,同时胼胝体中的星形胶质细胞水平和血清细胞因子水平会降低,合并暴露会导致胼胝体髓鞘化和血清皮质酮显著降低。男性血清皮质酮的减少与神经递质水平的减少相关,纹状体谷氨酸能功能的减少与胼胝体星形胶质细胞的减少特别相关。UFP诱导的男性神经递质水平的变化在产后暴露后得到缓解,这表明存在潜在的适应性,而皮质酮和胼胝体神经病理效应的降低在产后和青少年期的联合暴露中得到进一步加强。UFP诱导的女性变化主要发生在纹状体多巴胺系统,只有在产后和青春期联合暴露的情况下,血清细胞因子才会减少。对男性的研究结果凸显了对神经毒性机制进行更全面的生理评估的重要性。此外,这些研究结果还为不断积累的、将空气污染与神经发育和精神疾病联系起来的流行病学文献提供了生物学上的合理性。因此,这些研究结果支持有必要考虑对空气污染中的 UFP 成分进行调节。
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Male-biased vulnerability of mouse brain tryptophan/kynurenine and glutamate systems to adolescent exposures to concentrated ambient ultrafine particle air pollution

Air pollution (AP) exposures have been associated with numerous neurodevelopmental and psychiatric disorders, including autism spectrum disorder, attention deficit hyperactivity disorder and schizophrenia, all male-biased disorders with onsets from early life to late adolescence/early adulthood. While prior experimental studies have focused on effects of AP exposures during early brain development, brain development actually extends well into early adulthood. The current study in mice sought to extend the understanding of developmental brain vulnerability during adolescence, a later but significant period of brain development and maturation to the ultrafine particulate (UFPs) component of AP, considered its most reactive component. Additionally, it examined adolescent response to UFPs when preceded by earlier developmental exposures, to ascertain the trajectory of effects and potential enhancement or mitigation of adverse consequences. Outcomes focused on shared features associated with multiple neurodevelopmental disorders. For this purpose, C57Bl/6 J mice of both sexes were exposed to ambient concentrated UFPs or filtered air from PND (postnatal day) 4–7 and PND10–13, and again at PND39–42 and 45–49, resulting in 3 exposure postnatal/adolescent treatment groups per sex: Air/Air, Air/UFP, and UFP/UFP. Features common to neurodevelopmental disorders were examined at PND50. Mass exposure concentration from postnatal exposure averaged 44.34 μg/m3 and the adolescent exposure averaged 49.18 μg/m3. Male brain showed particular vulnerability to UFP exposures in adolescence, with alterations in frontal cortical and striatal glutamatergic and tryptophan/serotonergic neurotransmitters and concurrent reductions in levels of astrocytes in corpus callosum and in serum cytokine levels, with combined exposures resulting in significant reductions in corpus callosum myelination and serum corticosterone. Reductions in serum corticosterone in males correlated with reductions in neurotransmitter levels, and reductions in striatal glutamatergic function specifically correlated with reductions in corpus callosum astrocytes. UFP-induced changes in neurotransmitter levels in males were mitigated by prior postnatal exposure, suggesting potential adaptation, whereas reductions in corticosterone and in corpus callosum neuropathological effects were further strengthened by combined postnatal and adolescent exposures. UFP-induced changes in females occurred primarily in striatal dopamine systems and as reductions in serum cytokines only in response to combined postnatal and adolescent exposures. Findings in males underscore the importance of more integrated physiological assessments of mechanisms of neurotoxicity. Further, these findings provide biological plausibility for an accumulating epidemiologic literature linking air pollution to neurodevelopmental and psychiatric disorders. As such, they support a need for consideration of the regulation of the UFP component of air pollution.

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来源期刊
Neurotoxicology
Neurotoxicology 医学-毒理学
CiteScore
6.80
自引率
5.90%
发文量
161
审稿时长
70 days
期刊介绍: NeuroToxicology specializes in publishing the best peer-reviewed original research papers dealing with the effects of toxic substances on the nervous system of humans and experimental animals of all ages. The Journal emphasizes papers dealing with the neurotoxic effects of environmentally significant chemical hazards, manufactured drugs and naturally occurring compounds.
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