Innovative Vision Products Inc, County of New Castle, DE, USA.
Am J Ther. 2011 Nov;18(6):e209-26. doi: 10.1097/MJT.0b013e3181cf8ebb.
Globally, tobacco use is associated with 5 million deaths per annum and is regarded as one of the leading causes of premature death. Major chronic disorders associated with smoking include cardiovascular diseases, several types of cancer, and chronic obstructive pulmonary disease (lung problems). Cigarette smoking (CS) generates a cumulative oxidative stress, which may contribute to the pathogenesis of chronic diseases. Mainstream and side stream gas-phase smoke each have about the same concentration of reactive free radical species, about 1 × 10(16) radicals per cigarette (or 5 × 10(14) per puff). This effect is critical in understanding the biologic effects of smoke. Several lines of evidence suggest that cigarette smoke constituents can directly activate vascular reactive oxygen species production. In this work we present multiple evidence that CS provide the important risk factors in many age-related diseases, and is associated with increased cumulative and systemic oxidative stress and inflammation. The cited processes are marked by increased white blood cell (leucocytes, WBCs) turnover. The data suggest an alteration of the circulating WBCs by CS, resulting in increased adherence to endothelial cells. Telomeres are complex DNA-protein structures located at the end of eukaryotic chromosomes. Telomere length shortens with biologic age in all replicating somatic cells. It has been shown that tobacco smoking enhances telomere shortening in circulating human WBCs. Telomere attrition (expressed in WBCs) can serve as a biomarker of the cumulative oxidative stress and inflammation induced by smoking and, consequently, show the pace of biologic aging. We originally propose that patented specific oral formulations of nonhydrolized carnosine and carcinine provide a powerful tool for targeted therapeutic inhibition of cumulative oxidative stress and inflammation and protection of telomere attrition associated with smoking. The longitudinal studies of the clinical population groups described in this study including elderly support the hypothesis that telomere length is a predictor of survival and therapeutic treatment requirement associated with smoking behavior.
全球范围内，烟草使用每年导致 500 万人死亡，被认为是导致早逝的主要原因之一。与吸烟相关的主要慢性疾病包括心血管疾病、多种癌症和慢性阻塞性肺疾病（肺部问题）。吸烟会产生累积的氧化应激，这可能导致慢性疾病的发病机制。主流烟雾和侧流烟雾中的气相烟雾自由基浓度大致相同，每支香烟（或每口烟）约有 1×10（16）个自由基（或每口烟约有 5×10（14）个自由基）。这一效应在理解烟雾的生物学效应方面至关重要。有几条证据表明，香烟烟雾成分可以直接激活血管活性氧物质的产生。在这项工作中，我们提供了多个证据，表明香烟烟雾是许多与年龄相关疾病的重要危险因素，并且与累积性和全身性氧化应激和炎症的增加有关。这些过程的标志是白细胞（白细胞，WBC）周转率增加。数据表明，香烟烟雾改变了循环中的 WBC，导致其与内皮细胞的黏附增加。端粒是位于真核染色体末端的复杂 DNA-蛋白质结构。在所有复制的体细胞中，端粒长度随着生物年龄的增长而缩短。已经表明，吸烟会加速循环中的人类 WBC 端粒缩短。端粒磨损（在 WBC 中表达）可作为吸烟引起的累积氧化应激和炎症的生物标志物，因此显示了生物学衰老的速度。我们最初提出，非水解肌肽和卡尼丁的专利口服制剂为靶向治疗抑制累积氧化应激和炎症以及保护与吸烟相关的端粒磨损提供了有力工具。本研究中描述的临床人群纵向研究支持这样的假设，即端粒长度是与吸烟行为相关的生存和治疗需求的预测因子。
