Hemmati Ali Asghar, Alboghobeish Soheila, Ahangarpour Akram
Ahvaz Jundishapur University of Medical Sciences.
Monaldi Arch Chest Dis. 2018 Mar 23;88(1):903. doi: 10.4081/monaldi.2018.903.
Arsenic is a common environmental and occupational contaminant worldwide which can influence the development of respiratory diseases. In recent years, alteration in the lifestyle as well as food habits have led to increased consumption of food containing high levels of fat. The present study was designed to evaluate the effects of chronic exposure to a high-fat diet (HFD) on arsenic-induced damages and oxidative stress in the lung tissue of mice. This is the first study to reveal the effect of diet-induced obesity on arsenic-induced lung damages. Seventy-two male Naval Medical Research Institute (NMRI) mice were divided into six groups and fed an HFD or standard diet (SD) while being exposed to 25 or 50 ppm of arsenic through drinking water for 20 weeks. At the end of the experiment, the lung weight to body weight ratio; oxidative stress markers, nitrite level, and hydroxyproline content in the lung tissue; and lung histology were evaluated. The results demonstrated that arsenic exposure leads to a significant decrease in the glutathione level and catalase enzyme activity, and significantly increased reactive oxygen species, malondialdehyde, and nitrite level, but it did not affect the superoxide dismutase activity and hydroxyproline content in the lung tissue. Consequently, all the parameters studied aggravated when HFD was consumed along with arsenic. These findings were confirmed by histological examination. Our study showed that HFD increased arsenic-induced lung damages through oxidative stress in mice. These findings could be important for clinical research to protect against arsenic-induced respiratory toxicity in humans.
砷是一种在全球范围内常见的环境和职业污染物，可影响呼吸系统疾病的发展。近年来，生活方式和饮食习惯的改变导致高脂肪食物的摄入量增加。本研究旨在评估长期高脂饮食（HFD）对砷诱导的小鼠肺组织损伤和氧化应激的影响。这是第一项揭示饮食诱导的肥胖对砷诱导的肺损伤影响的研究。将72只雄性海军医学研究所（NMRI）小鼠分为六组，喂食高脂饮食或标准饮食（SD），同时通过饮用水接触25或50 ppm的砷，持续20周。实验结束时，评估肺重与体重比、肺组织中的氧化应激标志物、亚硝酸盐水平和羟脯氨酸含量以及肺组织学。结果表明，砷暴露导致谷胱甘肽水平和过氧化氢酶活性显著降低，活性氧、丙二醛和亚硝酸盐水平显著升高，但不影响肺组织中的超氧化物歧化酶活性和羟脯氨酸含量。因此，当高脂饮食与砷一起摄入时，所有研究参数都会加重。这些发现通过组织学检查得到证实。我们的研究表明，高脂饮食通过氧化应激增加了砷诱导的小鼠肺损伤。这些发现可能对预防人类砷诱导的呼吸毒性的临床研究具有重要意义。
