Lead‐induced neurodevelopmental lesion and epigenetic landscape: Implication in neurological disorders

Liu, Mengchen; Wang, Ruike; Ba, Yue; Yu, Fangfang; Deng, Qihong; Huang, Hui

doi:10.1002/jat.4419

Cited by 7 publications

(2 citation statements)

References 142 publications

(174 reference statements)

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“…In humans, PM in the form of black carbon was identified in cord blood and brain tissue derived from first and second trimester fetuses (Bongaerts et al., 2022; Bove et al., 2019), covering a significant period of development when microglia are first entering and proliferating in the brain (Menassa & Gomez‐Nicola, 2018). The pattern and timing of microglial activation therefore become critical especially as epidemiological studies linking neurodevelopmental disorders with early life PM exposure report different outcomes depending on point of exposure (Liu et al., 2023; Rahman et al., 2022).…”

Section: Discussionmentioning

confidence: 99%

Exposure to urban particulate matter (UPM) impairs mitochondrial dynamics in BV2 cells, triggering a mitochondrial biogenesis response

Morris,

Counsell,

McGonnell

et al. 2024

The Journal of Physiology

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World Health Organisation data suggest that up to 99% of the global population are exposed to air pollutants above recommended levels. Impacts to health range from increased risk of stroke and cardiovascular disease to chronic respiratory conditions, and air pollution may contribute to over 7 million premature deaths a year. Additionally, mounting evidence suggests that in utero or early life exposure to particulate matter (PM) in ambient air pollution increases the risk of neurodevelopmental impairment with obvious lifelong consequences. Identifying brain‐specific cellular targets of PM is vital for determining its long‐term consequences. We previously established that microglial‐like BV2 cells were particularly sensitive to urban (U)PM‐induced damage including reactive oxygen species production, which was abrogated by a mitochondrially targeted antioxidant. Here we extend those studies to find that UPM treatment causes a rapid impairment of mitochondrial function and increased mitochondrial fragmentation. However, there is a subsequent restoration of mitochondrial and therefore cell health occurring concomitantly with upregulated measures of mitochondrial biogenesis and mitochondrial load. Our data highlight that protecting mitochondrial function may represent a valuable mechanism to offset the effects of UPM exposure in the neonatal brain. imageKey points Air pollution represents a growing risk to long‐term health especially in early life, and the CNS is emerging a target for airborne particulate matter (PM). We previously showed that microglial‐like BV2 cells were vulnerable to urban (U)PM exposure, which impaired cell survival and promoted reactive oxygen species production. Here we find that, following UPM exposure, BV2 mitochondrial membrane potential is rapidly reduced, concomitant with decreased cellular bioenergetics and increased mitochondrial fission. However, markers of mitochondrial biogenesis and mitochondrial mass are subsequently induced, which may represent a cellular mitigation strategy. As mitochondria are more vulnerable in the developing brain, exposure to air pollution may represent a greater risk to lifelong health in this cohort; conversely, promoting mitochondrial integrity may offset these risks.

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Section: Discussionmentioning

confidence: 99%

Exposure to urban particulate matter (UPM) impairs mitochondrial dynamics in BV2 cells, triggering a mitochondrial biogenesis response

Morris,

Counsell,

McGonnell

et al. 2024

The Journal of Physiology

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“…Besides being the cause of "itai-itai" disease, chronic cadmium exposure may lead to irreversible renal failure [5,6]. Multiple studies have also discovered that lead adversely influences children's neurodevelopment [7,8].…”

Section: Introductionmentioning

confidence: 99%

Pollution Profiles, Source Identification and Health Risk Assessment of Heavy Metals in Soil near a Non-Ferrous Metal Smelting Plant

Zhang

et al. 2023

IJERPH

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Heavy metal pollution related to non-ferrous metal smelting may pose a significant threat to human health. This study analyzed 58 surface soils collected from a representative non-ferrous metal smelting area to screen potentially hazardous heavy metals and evaluate their health risk in the studied area. The findings demonstrated that human activity had contributed to the pollution degrees of Cu, Cd, As, Zn, and Pb in the surrounding area of a non-ferrous metal smelting plant (NMSP). Cu, Cd, As, Zn, Pb, Ni, and Co pollution within the NMSP was serious. Combining the spatial distribution and Spearman correlations with principal component analysis (PCA), the primary sources of Cd, As, Pb, and Zn in surrounding areas were related to non-ferrous metal smelting and transportation activities. High non-cancer (THI = 4.76) and cancer risks (TCR = 2.99 × 10−4) were found for adults in the NMSP. Moreover, heavy metals in the surrounding areas posed a potential cancer risk to children (TCR = 3.62 × 10−6) and adults (TCR = 1.27 × 10−5). The significant contributions of As, Pb, and Cd to health risks requires special attention. The construction of a heavy metal pollution management system will benefit from the current study for the non-ferrous metal smelting industry.

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Dynamic alterations of locomotor activity and the microbiota in zebrafish larvae with low concentrations of lead exposure

Xia,

Li,

Wang

et al. 2023

Environ Sci Pollut Res

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Lead‐induced neurodevelopmental lesion and epigenetic landscape: Implication in neurological disorders

Cited by 7 publications

References 142 publications

Exposure to urban particulate matter (UPM) impairs mitochondrial dynamics in BV2 cells, triggering a mitochondrial biogenesis response

Exposure to urban particulate matter (UPM) impairs mitochondrial dynamics in BV2 cells, triggering a mitochondrial biogenesis response

Pollution Profiles, Source Identification and Health Risk Assessment of Heavy Metals in Soil near a Non-Ferrous Metal Smelting Plant

Dynamic alterations of locomotor activity and the microbiota in zebrafish larvae with low concentrations of lead exposure

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