{"title":"Changes of zinc, copper, and iron levels in the lung of male rats after subacute (4-week) and subchronic (13-week) exposure to formaldehyde","authors":"Og̊uz Aslan Özen, Ahmet Songur, Mustafa Sarsılmaz, Mehmet Yaman, İlter Kuş","doi":"10.1002/jtra.10026","DOIUrl":null,"url":null,"abstract":"The medical use of formaldehyde has focused especially on laboratory use. Harmful effects of formaldehyde inhalation, such as nasal squamous cell carcinoma, are quite well documented. However, detailed studies of the mechanisms of the damaging effects of formaldehyde on lung tissue are quite limited. Amounts of such elements as zinc, copper, and iron within lung tissue indicate whether or not they function physiologically. In this study, 36 adult albino Wistar male rats (6 animals per group) were exposed to 0 (Control), 5, and 10 ppm (1 ppm ≊ 1.2 mg/m3) of formaldehyde gas for subacute (4-week) and subchronic (13-week) periods. Whole-body exposure was continuously carried out for 8 h/day, 5 days/week. Body weights were recorded weekly. Levels of metals mentioned above were measured in lung tissue by atomic absorption spectrometry using wet ashing and were then compared with levels in the control groups. At the end of the study, a gradual decrease in weight gain, a decrease in zinc levels, and an increase in iron levels were observed in both subacute and subchronic groups compared to control groups. Statistically significant increases in tissue Fe levels were seen in the 10 ppm subacute (P < 0.001), 5 ppm subchronic (P < 0.001), and 10 ppm subchronic (P < 0.001) groups. We conclude that subacute or subchronic exposure to cytotoxic concentrations of formaldehyde may cause growth retardation and alter the trace element levels of zinc and iron in the lung tissue. J. Trace Elem. Exp. Med. 16:67–74, 2003. © 2003 Wiley-Liss, Inc.","PeriodicalId":101243,"journal":{"name":"The Journal of Trace Elements in Experimental Medicine","volume":"16 2-3","pages":"67-74"},"PeriodicalIF":0.0000,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1002/jtra.10026","citationCount":"5","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"The Journal of Trace Elements in Experimental Medicine","FirstCategoryId":"1085","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/jtra.10026","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 5
亚急性(4周)和亚慢性(13周)暴露于甲醛后雄性大鼠肺中锌、铜和铁水平的变化
甲醛的医学用途尤其集中在实验室使用上。吸入甲醛的有害影响,如鼻鳞状细胞癌,已经有了很好的记录。然而,对甲醛对肺组织损伤作用机制的详细研究相当有限。肺组织中锌、铜和铁等元素的量表明它们是否具有生理功能。在这项研究中,36只成年白化Wistar雄性大鼠(每组6只)暴露于0(对照)、5和10ppm(1ppm≊1.2 mg/m3)的甲醛气体中,持续亚急性(4周)和亚慢性(13周)。全身暴露持续进行8小时/天,5天/周。每周记录体重。通过使用湿灰化的原子吸收光谱法测量肺组织中上述金属的水平,然后将其与对照组中的水平进行比较。研究结束时,与对照组相比,亚急性组和亚慢性组的体重增加逐渐减少,锌水平下降,铁水平增加。在亚急性10ppm(P<;0.001)、亚慢性5ppm(P>;0.001)和亚慢性10ppm(P/lt;0.001。我们得出的结论是,亚急性或亚慢性暴露于细胞毒性浓度的甲醛可能会导致生长迟缓,并改变肺组织中锌和铁的微量元素水平。J.Trace Elem。Exp.Med.16:67-742003。©2003 Wiley-Liss,股份有限公司。
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