Manti Sara, Marseglia Lucia, D'Angelo Gabriella, Cuppari Caterina, Cusumano Erika, Arrigo Teresa, Gitto Eloisa, Salpietro Carmelo
Unit of Pediatric Genetics and Immunology, Department of Pediatrics, University of Messina, 98125 Messina, Italy.
Neonatal and Pediatric Intensive Care Unit, Department of Pediatrics, University of Messina, 98125 Messina, Italy.
Oxid Med Cell Longev. 2016;2016:8651820. doi: 10.1155/2016/8651820. Epub 2016 Jul 18.
Although extensive epidemiological and laboratory studies have been performed to identify the environmental and immunological causes of atopy, genetic predisposition seems to be the biggest risk factor for allergic diseases. The onset of atopic diseases may be the result of heritable changes of gene expression, without any alteration in DNA sequences occurring in response to early environmental stimuli. Findings suggest that the establishment of a peculiar epigenetic pattern may also be generated by oxidative stress (OS) and perpetuated by the activation of OS-related genes. Analyzing the role of maternal and neonatal oxidative stress and oxidative stress-inducible genes, the purpose of this review was to summarize what is known about the relationship between maternal and neonatal OS-related genes and the development of atopic diseases.
尽管已经进行了广泛的流行病学和实验室研究来确定特应性的环境和免疫原因，但遗传易感性似乎是过敏性疾病的最大风险因素。特应性疾病的发病可能是基因表达可遗传变化的结果，而不会因早期环境刺激导致DNA序列发生任何改变。研究结果表明，特殊表观遗传模式的建立也可能由氧化应激（OS）产生，并通过激活与OS相关的基因得以延续。通过分析母体和新生儿氧化应激以及氧化应激诱导基因的作用，本综述旨在总结关于母体和新生儿与OS相关基因以及特应性疾病发展之间关系的已知情况。
