內(nèi)穆爾兒童癌癥研究中心主任A. K. Rajasekaran博士領(lǐng)導(dǎo)的研究小組完成的一項研究表明,，香煙煙霧中的一種物質(zhì)停止參與細胞功能和調(diào)節(jié)的一個關(guān)鍵蛋白質(zhì),。研究論文發(fā)表在《美國生理學(xué)雜志-肺癌細胞和分子生理學(xué)》上。
香煙煙霧被確認(rèn)為是肺癌以及成人許多其他形式癌癥的致病因素,。香煙煙霧中有4000多個成分,，其中許多都與肺癌的發(fā)生發(fā)展有關(guān)。有證據(jù)表明二手煙與一手煙一樣,，同樣?對人體細胞有影響,。
在這項研究中，研究人員發(fā)現(xiàn)煙煙霧中一種稱為活性氧（ROS）的致癌劑,，ROS能抑制正常細胞的功能,。暴露于兩支香煙產(chǎn)生的二手煙環(huán)境下，發(fā)現(xiàn)細胞的鈉泵在幾個小時內(nèi)幾乎完全喪失功能,。
在正常細胞中,，鈉泵起著至關(guān)重要的作用，運送鉀到細胞,、運輸鈉出細胞,。細胞的鈉泵功能的受損，將導(dǎo)致細胞損傷,、病情惡化并最終影響生存,。
Rajasekaran博士說：我們現(xiàn)在知道吸入二手煙顆粒物同樣也會遭受吸煙帶來的后果。當(dāng)你呼吸時,，假如站在吸煙者的附近暴露于氣態(tài)物質(zhì)下,，這足以能造成傷害。
加州大學(xué)洛杉磯分校病理學(xué)和實驗室醫(yī)學(xué)系副教授,、文章作者Lee Goodglic博士指出：目前,，很少有可靠的肺腫瘤標(biāo)志物可以預(yù)測生存、治療方案或治療反應(yīng),。只有少數(shù)幾個已知的被確認(rèn)有預(yù)測功能的生物標(biāo)志物,。而研究發(fā)現(xiàn)鈉泵可以作為肺癌新的生物標(biāo)志物,。
這項研究保護兒童免于暴露于香煙煙霧環(huán)境下提供了新證據(jù)。在兒童成長過程中,，童年時過度暴露于香煙煙霧環(huán)境下可能會促進肺癌的發(fā)展,。
要了解香煙煙霧抑制鈉泵產(chǎn)生的后果還需開展更多相關(guān)研究，但至少這項研究表明二手煙的危害可能比我們以前想象的那樣更危險,。（生物谷：Bioon）
doi:10.1152/ajplung.00384.2010
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Na,K-ATPase is a target of cigarette smoke and reduced expression predicts poor patient outcome of smokers with lung cancer
T. P. Huynh, V. Mah, V. B. Sampson, D. Chia, M. C. Fishbein, S. Horvath, M. Alavi, D. C. Wu, J. Harper, T. Sarafian, S. M. Dubinett, S. A. Langhans, L. Goodglick, A. 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.
