The Toxicological Mechanisms of Environmental Soot (Black Carbon) and Carbon Black: Focus on Oxidative Stress and Inflammatory Pathways.
The Toxicological Mechanisms of Environmental Soot (Black Carbon) and Carbon Black: Focus on Oxidative Stress and Inflammatory Pathways.
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DOI：
10.3389/fimmu.2017.00763
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发表时间：
2017
影响因子：
7.3
通讯作者：
Thakur AK
中科院分区：
文献类型：
--
作者：
Niranjan R;Thakur AK
环境烟尘和碳黑(CBS)可导致多种疾病，但其潜在的毒性机制尚不清楚。两者都是在碳氢化合物不完全燃烧后形成的，但它们的组成和碳含量的百分比不同。帕西瓦尔·波特爵士首次将烟尘描述为致癌物质，随后许多其他人证实了这一点。现有数据表明，煤烟和CB暴露导致的疾病主要有三种：癌症、呼吸系统疾病和心血管功能障碍。实验模型揭示了氧化应激、DNA甲基化、DNA加合物的形成和芳烃受体激活是烟尘和CB诱发癌症的关键机制。煤烟中的硅、铁、锰、钛和钴等金属也参与了活性氧(ROS)介导的DNA损伤。从机理上讲，ROS诱导的DNA损伤进一步被嗜酸性粒细胞和中性粒细胞通过依赖卤化物(Cl−和BrDNA−)的DNA加合物的形成所增强。肺树突状细胞、辅助性T细胞2型和肥大细胞的激活在煤烟或CB诱导的呼吸系统疾病的病理过程中是重要的中介细胞。多不饱和脂肪酸(PUFAs)也被发现在呼吸系统疾病中调节T细胞功能。特别是，端粒酶逆转录酶被发现在煤烟和CB诱导的心血管功能障碍中起关键作用。在这篇综述中，我们提出了煤烟和CB诱导的毒性的综合机制，强调了炎症介质和氧化应激的作用。我们还建议使用抗氧化剂和多不饱和脂肪酸作为预防煤烟和CB诱导的疾病的保护策略。
The environmental soot and carbon blacks (CBs) cause many diseases in humans, but their underlying mechanisms of toxicity are still poorly understood. Both are formed after the incomplete combustion of hydrocarbons but differ in their constituents and percent carbon contents. For the first time, “Sir Percival Pott” described soot as a carcinogen, which was subsequently confirmed by many others. The existing data suggest three main types of diseases due to soot and CB exposures: cancer, respiratory diseases, and cardiovascular dysfunctions. Experimental models revealed the involvement of oxidative stress, DNA methylation, formation of DNA adducts, and Aryl hydrocarbon receptor activation as the key mechanisms of soot- and CB-induced cancers. Metals including Si, Fe, Mn, Ti, and Co in soot also contribute in the reactive oxygen species (ROS)-mediated DNA damage. Mechanistically, ROS-induced DNA damage is further enhanced by eosinophils and neutrophils via halide (Cl− and Br−) dependent DNA adducts formation. The activation of pulmonary dendritic cells, T helper type 2 cells, and mast cells is crucial mediators in the pathology of soot- or CB-induced respiratory disease. Polyunsaturated fatty acids (PUFAs) were also found to modulate T cells functions in respiratory diseases. Particularly, telomerase reverse transcriptase was found to play the critical role in soot- and CB-induced cardiovascular dysfunctions. In this review, we propose integrated mechanisms of soot- and CB-induced toxicity emphasizing the role of inflammatory mediators and oxidative stress. We also suggest use of antioxidants and PUFAs as protective strategies against soot- and CB-induced disorders.
影响因子：
10
作者：
Eder C;Frankenberger M;Stanzel F;Seidel A;Schramm KW;Ziegler-Heitbrock L;Hofer TP
通讯作者：
Hofer TP