Maternal exposure to polystyrene nanoplastics alters fetal brain metabolism in mice

Mercer, Grace V.; Harvey, Nikita E.; Steeves, Katherine L.; Schneider, Céline M.; Sled, John G.; Macgowan, Christopher K.; Baschat, Ahmet A.; Kingdom, John C.; Simpson, André J.; Simpson, Myrna J.; Jobst, Karl J.; Cahill, Lindsay S.

doi:10.1007/s11306-023-02061-3

Cited by 8 publications

(2 citation statements)

References 43 publications

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“…和神经元细胞活性降低 [98] . 将受孕母鼠暴露于聚苯乙烯微塑料环境中, 发现暴露组胎儿大脑内的神经递质γ-氨基丁酸和葡萄糖等营养物质的相对浓度分别降低了40% 和30%(P<0.05), 说明微塑料会干扰胎儿大脑的正常代谢 [99] . 利用生物素示踪技术定性暴露于聚苯乙烯的小鼠脑部微塑料蓄积状态, 结果显示, 微塑料主要集中在海马体、下丘脑和皮层; 暴露组小鼠水迷宫实验显示, 小鼠寻找隐藏平台的时间普遍高于对照组, 说明聚苯乙烯纳米颗粒对小鼠的学习和记忆功能造成损伤 [100] .…”

Section: 倾向于流入下丘脑、髓质等内脑区域并蓄积部分unclassified

Effects of environmental stress on human brain development and its mechanisms

Liu,

Zhao,

Wang

et al. 2024

Chin. Sci. Bull.

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Section: 倾向于流入下丘脑、髓质等内脑区域并蓄积部分unclassified

Effects of environmental stress on human brain development and its mechanisms

Liu,

Zhao,

Wang

et al. 2024

Chin. Sci. Bull.

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“…MNPLs have been identified in amniotic fluid during pregnancy [101]. A recent high-resolution ex vivo MRI study in mice revealed brain abnormalities, including in the motor cortex and corpus callosum (both predominantly involved in ALS), following maternal exposure to polystyrene nanoplastics [102]. Overall there is mounting evidence that exposure to MNPLs is detrimental during the perinatal period, particularly through ingestion, and can cause toxicity specifically in primary motor neurons by activating an oxidative stress response and inducing apoptosis, consequently impairing motor performance [103].…”

Section: Mnpl Neonatal Toxicitymentioning

confidence: 99%

Nanoplastics and Neurodegeneration in ALS

Eisen,

Pioro,

Goutman

et al. 2024

Brain Sciences

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Plastic production, which exceeds one million tons per year, is of global concern. The constituent low-density polymers enable spread over large distances and micro/nano particles (MNPLs) induce organ toxicity via digestion, inhalation, and skin contact. Particles have been documented in all human tissues including breast milk. MNPLs, especially weathered particles, can breach the blood–brain barrier, inducing neurotoxicity. This has been documented in non-human species, and in human-induced pluripotent stem cell lines. Within the brain, MNPLs initiate an inflammatory response with pro-inflammatory cytokine production, oxidative stress with generation of reactive oxygen species, and mitochondrial dysfunction. Glutamate and GABA neurotransmitter dysfunction also ensues with alteration of excitatory/inhibitory balance in favor of reduced inhibition and resultant neuro-excitation. Inflammation and cortical hyperexcitability are key abnormalities involved in the pathogenic cascade of amyotrophic lateral sclerosis (ALS) and are intricately related to the mislocalization and aggregation of TDP-43, a hallmark of ALS. Water and many foods contain MNPLs and in humans, ingestion is the main form of exposure. Digestion of plastics within the gut can alter their properties, rendering them more toxic, and they cause gut microbiome dysbiosis and a dysfunctional gut–brain axis. This is recognized as a trigger and/or aggravating factor for ALS. ALS is associated with a long (years or decades) preclinical period and neonates and infants are exposed to MNPLs through breast milk, milk substitutes, and toys. This endangers a time of intense neurogenesis and establishment of neuronal circuitry, setting the stage for development of neurodegeneration in later life. MNPL neurotoxicity should be considered as a yet unrecognized risk factor for ALS and related diseases.

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