A Health Threat to Bystanders Living in the Homes of Smokers: How Smoke Toxins Deposited on Surfaces Can Cause Insulin Resistance.
A Health Threat to Bystanders Living in the Homes of Smokers: How Smoke Toxins Deposited on Surfaces Can Cause Insulin Resistance.
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DOI：
10.1371/journal.pone.0149510
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Martins Green M
中科院分区：
文献类型：
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作者：
Adhami N;Starck SR;Flores C;Martins Green M
三手烟（Thirdhand Smoke，THS）是指二手烟在环境表面的积聚。THS存在于吸烟者的衣服和头发上，以及吸烟者的家庭和汽车表面。接触通过摄入、吸入和皮肤吸收发生。生活在吸烟者家中的儿童面临的风险最高，因为他们在地板上爬行，触摸父母的衣服/头发和家用物品。使用小鼠暴露于THS的条件下，模拟暴露的人类，我们表明，THS增加细胞的氧化应激，通过增加超氧化物歧化酶（SOD）的活性和过氧化氢（H2 O2）的水平，同时降低抗氧化酶的活性过氧化氢酶和谷胱甘肽过氧化物酶（GPx），分解成H2O和O2的H2 O2。这导致脂质过氧化、蛋白质亚硝基化和DNA损伤。这些细胞和分子变化的后果是高血糖症和胰岛素血症。事实上，我们发现胰岛素受体、PI 3 K、AKT的水平降低，这些都是胰岛素信号传导和细胞摄取葡萄糖的重要分子。为了确定这些对THS诱导的胰岛素抵抗的影响是否是由于氧化应激的增加，我们用抗氧化剂N-乙酰半胱氨酸（NAC）和α-生育酚（alpha-toc）处理暴露于THS的小鼠，并显示氧化应激，分子损伤和胰岛素抵抗显著逆转。相反，给小鼠喂食模拟“西方饮食”的食物（已知会增加氧化应激），同时将小鼠暴露于THS，会进一步增加氧化应激并加剧高血糖症和胰岛素血症。总之，THS暴露通过氧化应激导致非肥胖II型糖尿病（NODII）形式的胰岛素抵抗。如果在人类中得到证实，这些研究可能会对人们如何看待暴露于环境烟草毒素产生重大影响，特别是对儿童，老年人和烟草烟雾环境中的工人。
Thirdhand smoke (THS) is the accumulation of secondhand smoke on environmental surfaces. THS is found on the clothing and hair of smokers as well as on surfaces in homes and cars of smokers. Exposure occurs by ingestion, inhalation and dermal absorption. Children living in homes of smokers are at highest risk because they crawl on the floor, touch parents’ clothing/hair and household objects. Using mice exposed to THS under conditions that mimic exposure of humans, we show that THS increases cellular oxidative stress by increasing superoxide dismutase (SOD) activity and hydrogen peroxide (H2O2) levels while reducing the activity of antioxidant enzymes catalase and glutathione peroxidase (GPx) that break down H2O2 into H2O and O2. This results in lipid peroxidation, protein nitrosylation and DNA damage. Consequences of these cell and molecular changes are hyperglycemia and insulinemia. Indeed, we found reduced levels of insulin receptor, PI3K, AKT, all important molecules in insulin signaling and glucose uptake by cells. To determine whether these effects on THS-induced insulin resistance are due to increase in oxidative stress, we treated mice exposed to THS with the antioxidants N-acetyl cysteine (NAC) and alpha-tocopherol (alpha-toc) and showed that the oxidative stress, the molecular damage, and the insulin resistance, were significantly reversed. Conversely, feeding the mice with chow that mimics “western diet”, which is known to increase oxidative stress, while exposing the mice to THS, further increased the oxidative stress and aggravated hyperglycemia and insulinemia. In conclusion, THS exposure results in insulin resistance in the form of non-obese type II diabetes (NODII) through oxidative stress. If confirmed in humans, these studies could have a major impact on how people view exposure to environmental tobacco toxins, in particular to children, elderly and workers in environments where tobacco smoke has taken place.