空气污染引起的神经毒性:空气污染,表观遗传变化和神经疾病之间的关系
Sebastian Kalenik1,2, Agnieszka Zaczek1, Aleksandra Rodacka1
1Department of Oncobiology and Epigenetics, Faculty of Biology and Environmental Protection, University of Lodz, 141/143 Pomorska Street, 90-236 Lodz, Poland.
International journal of molecular sciences
|April 17, 2025
概括
空气污染导致全球数百万人死亡,并与神经退行性疾病有关. 新兴研究表明,空气污染物可能会引发表观遗传变化,影响大脑健康和疾病发展.
科学领域:
- 环境健康 环境健康
- 神经科学是一个神经科学.
- 毒理学 毒理学 毒理学
背景情况:
- 空气污染是一个重大的全球健康问题,每年造成数百万人的死亡,并导致各种疾病.
- 颗粒物 (PM) 是一种主要的空气污染物,由于其复杂的组成和到达深层组织的能力,包括大脑,因此构成重大风险.
- 现有的研究将空气污染与神经发育和神经退行性疾病联系起来,但确切的机制尚不清楚.
研究的目的:
- 探索空气污染与神经疾病之间的联系.
- 研究由空气污染物诱导的表观遗传变化在神经毒性的潜在作用.
- 了解空气污染如何影响与大脑功能和疾病相关的基因表达.
主要方法:
- 审查有关空气污染,颗粒物和神经系统疾病的现有文献.
- 对调查空气污染神经毒性影响的生物机制的研究进行分析,包括氧化应激,炎症和兴奋毒性.
- 检查空气污染引起的表观遗传修饰及其对基因表达的潜在影响的研究.
主要成果:
- 空气污染,特别是颗粒物,与呼吸道,心血管和神经系统疾病的风险增加有关.
- 颗粒物可以穿过血脑屏障,导致神经毒性.
- 有证据表明,空气污染引发了表观遗传变化,改变了与神经健康相关的基因表达.
结论:
- 空气污染是神经系统疾病的关键环境风险因素.
- 表观遗传修饰代表了空气污染影响中枢神经系统的潜在机制.
- 对污染物特异性表观遗传变化的进一步研究可以促进神经疾病的早期检测和管理.
相关概念视频
Types of Toxins
1.4K
Humans continually engage with an environment rich in potentially harmful chemicals. These are introduced to our bodies through inhalation, ingestion, or skin contact. These chemicals exist in various forms, such as air and environmental pollutants, agricultural chemicals, organic solvents, and heavy metals.
Air pollutants, primarily gases, pose significant threats to respiratory health, leading to conditions like hypoxia, lung cancer, and in extreme cases, death.
Environmental pollutants like...
Air pollutants, primarily gases, pose significant threats to respiratory health, leading to conditions like hypoxia, lung cancer, and in extreme cases, death.
Environmental pollutants like...
1.4K
Epigenetic Regulation
30.7K
Epigenetic mechanisms play an essential role in healthy development. Conversely, precisely regulated epigenetic mechanisms are disrupted in diseases like cancer.
30.7K
Disorders of the Nervous Tissue
940
Nervous tissue is a vital component of the human body's communication system, enabling us to perceive and respond to stimuli. However, like all other tissues, it is vulnerable to disorders and diseases that can significantly impact our neurological functioning.
Homeostatic Imbalances:
Alzheimer's disease manifests as a gradual decline in memory and cognitive abilities, attributed to the buildup of amyloid plaques and neurofibrillary tangles in the brain.
Parkinson's disease arises...
Homeostatic Imbalances:
Alzheimer's disease manifests as a gradual decline in memory and cognitive abilities, attributed to the buildup of amyloid plaques and neurofibrillary tangles in the brain.
Parkinson's disease arises...
940
Attention-Deficit/Hyperactivity Disorder
23
Attention-deficit/hyperactivity disorder (ADHD) is a neurodevelopmental disorder characterized by persistent inattention, hyperactivity, and impulsivity. It affects approximately 5-8% of children globally, with around 60-70% of cases persisting into adulthood. ADHD has significant implications for educational attainment, social interactions, and occupational success.
Diagnostic Criteria and Symptoms
To diagnose ADHD, symptoms must manifest before age 12 and be evident across multiple settings....
Diagnostic Criteria and Symptoms
To diagnose ADHD, symptoms must manifest before age 12 and be evident across multiple settings....
23
Drugs Affecting Neurotransmitter Synthesis
1.2K
Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase,...
1.2K
Chronic Obstructive Pulmonary Disease-II: Pathophysiology
2.7K
Chronic Obstructive Pulmonary Disease (COPD) pathophysiology is intricate and multifaceted, involving a complex interplay of physiological processes. Understanding these mechanisms is crucial for effectively managing and treating COPD. Here is an in-depth look at the critical elements in the pathophysiology of COPD:
Chronic Inflammation
Chronic Inflammation
2.7K


