Hoffman Jessie B, Petriello Michael C, Hennig Bernhard
Rev Environ Health. 2017 Mar 1;32(1-2):65-72. doi: 10.1515/reveh-2016-0041.
Exposure to environmental pollutants is a global health problem and is associated with the development of many chronic diseases, including cardiovascular disease, diabetes and metabolic syndrome. There is a growing body of evidence that nutrition can both positively and negatively modulate the toxic effects of pollutant exposure. Diets high in proinflammatory fats, such as linoleic acid, can exacerbate pollutant toxicity, whereas diets rich in bioactive and anti-inflammatory food components, including omega-3 fatty acids and polyphenols, can attenuate toxicant-associated inflammation. Previously, researchers have elucidated direct mechanisms of nutritional modulation, including alteration of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling, but recently, increased focus has been given to the ways in which nutrition and pollutants affect epigenetics. Nutrition has been demonstrated to modulate epigenetic markers that have been linked either to increased disease risks or to protection against diseases. Overnutrition (i.e. obesity) and undernutrition (i.e. famine) have been observed to alter prenatal epigenetic tags that may increase the risk of offspring developing disease later in life. Conversely, bioactive food components, including curcumin, have been shown to alter epigenetic markers that suppress the activation of NF-κB, thus reducing inflammatory responses. Exposure to pollutants also alters epigenetic markers and may contribute to inflammation and disease. It has been demonstrated that pollutants, via epigenetic modulations, can increase the activation of NF-κB and upregulate microRNAs associated with inflammation, cardiac injury and oxidative damage. Importantly, recent evidence suggests that nutritional components, including epigallocatechin gallate (EGCG), can protect against pollutant-induced inflammation through epigenetic regulation of proinflammatory target genes of NF-κB. Further research is needed to better understand how nutrition can modulate pollutant toxicity through epigenetic regulation. Therefore, the objective of this review is to elucidate the current evidence linking epigenetic changes to pollutant-induced diseases and how this regulation may be modulated by nutrients allowing for the development of future personalized lifestyle interventions.
接触环境污染物是一个全球性的健康问题,与许多慢性疾病的发生有关,包括心血管疾病、糖尿病和代谢综合征。越来越多的证据表明,营养既能积极地也能消极地调节污染物暴露的毒性作用。富含促炎脂肪(如亚油酸)的饮食会加剧污染物毒性,而富含生物活性和抗炎食物成分(包括ω-3脂肪酸和多酚)的饮食则可以减轻与毒物相关的炎症。此前,研究人员已经阐明了营养调节的直接机制,包括活化B细胞核因子κB(NF-κB)信号通路的改变,但最近,人们越来越关注营养和污染物影响表观遗传学的方式。营养已被证明可以调节与疾病风险增加或疾病预防相关的表观遗传标记。人们观察到营养过剩(即肥胖)和营养不足(即饥荒)会改变产前表观遗传标签,这可能会增加后代日后患疾病的风险。相反,包括姜黄素在内的生物活性食物成分已被证明可以改变表观遗传标记,抑制NF-κB的激活,从而减少炎症反应。接触污染物也会改变表观遗传标记,并可能导致炎症和疾病。已经证明,污染物通过表观遗传调节,可以增加NF-κB的激活,并上调与炎症、心脏损伤和氧化损伤相关的微小RNA。重要的是,最近的证据表明,包括表没食子儿茶素没食子酸酯(EGCG)在内的营养成分,可以通过对NF-κB促炎靶基因的表观遗传调控来预防污染物诱导的炎症。需要进一步研究以更好地理解营养如何通过表观遗传调控调节污染物毒性。因此,本综述的目的是阐明将表观遗传变化与污染物诱导疾病联系起来的现有证据,以及这种调节如何可能被营养物质调节,从而为未来个性化生活方式干预措施的开发提供依据。