导读：烟民吞云吐雾快活似神仙，健康问题往往不在考虑之中，身旁的不吸烟者尤其是小孩则深受二手烟之害。一项新的研究表明，二手烟中的物质会几乎完全停止一种参与细胞功能与调节的关键蛋白质的功能。
内穆尔儿童癌症研究中心的A. K. Rajasekaran博士所领导的一项研究显示，一种参与细胞功能与调节的关键蛋白可受香烟烟雾中一种物质的抑制。
人们对吸烟作为肺癌的诱因及与许多其他成年人癌症间的关联有着深刻的认识。吸烟产生烟雾中含有超过4000种组分，其中许多与肺癌的发生及恶化有关。证据表明，二手烟由于其对机体细胞的影响而具有同一手烟相同的危害性。
在该研究中，研究人员发现，在香烟烟雾中的一类叫做活性氧(ROS)的致癌物质具有抑制正常细胞功能的能力。研究发现，暴露在由两只香烟所产生的二手烟中数小时即可几乎完全停止细胞的钠离子泵功能。
在正常细胞中，钠离子泵在将钠离子运输进出细胞过程中发挥关键作用。细胞的钠离子泵性能（例如钠离子调节功能失效）可预示细胞损伤、疾病恶化以及细胞最终是否能存活。
“这是有关二手烟的一个重要的信息，”领导这项研究的Rajasekaran博士说。“我们现在知道人们无需吸入二手烟中的颗粒物质也会遭受吸烟的恶果。站在一个烟民旁边，那些气体物质就足以造成身体上的危害了。”
该研究作为最新成果，提供了证据支持保护儿童免于暴露在香烟烟雾中。小孩在孩童期过渡暴露于香烟烟雾中会促进成年时肺癌的发生。
要了解香烟烟雾抑制钠离子泵所造成的后果还需要开展更多的研究，不过该研究已经揭示，二手烟可能我们此前想象的更为危险。
Na,K-ATPase is a target of cigarette smoke and reduced expression predicts poor patient outcome of smokers with lung cancer
Thu P. Huynh, Vei Mah, Valerie B. Sampson, David Chia, Michael C. Fishbein, Steve Horvath, Mohammad Alavi, Debbie C. Wu, Jeffrey Harper, Ted Sarafian, Steven M. Dubinett, Sigrid A. Langhans, Lee Goodglick, and Ayyappan K Rajasekaran
Diminished Na,K-ATPase expression has been reported in several carcinomas and has been linked to tumor progression. However, few studies have determined if Na,K-ATPase function and expression are altered in lung malignancies. Since cigarette smoke (CS) is a major factor underlying lung carcinogenesis and progression, we investigated if CS affects Na,K-ATPase activity and expression in lung cells. Lung cells exposed to CS in vitro showed a reduction of Na,K-ATPase activity. We detected the presence of reactive oxygen species (ROS) in cells exposed to CS prior to Na,K-ATPase inhibition and neutralization of ROS restored Na,K-ATPase activity. We further determined whether Na,K-ATPase expression correlated with increasing grades of lung adenocarcinoma and survival of patients with smoking history. Immunohistochemical analysis of lung adenocarcinoma tissues revealed reduced Na,K-ATPase expression with increasing tumor grade. Using tissue microarray containing lung adenocarcinomas of patients with known smoking status, we found that high expression of Na,K-ATPase correlated with better survival. For the first time, these data demonstrate that CS is associated with loss of Na,K-ATPase function and expression in lung carcinogenesis, which might contribute to disease progression.
