de Oliveira Túlio Henrique Versiani, Campos Keila Karine Duarte, Soares Nícia Pedreira, Pena Karina Braga, Lima Wanderson Geraldo, Bezerra Frank Silva
Graduating in Medicine, School of Medicine, Federal University of Ouro Preto (UFOP), Ouro Preto, Minas Gerais, Brazil.
Department of Biological Sciences (DECBI), Laboratory of Metabolic Biochemistry (LBM), Center of Research in Biological Sciences (NUPEB), Federal University of Ouro Preto (UFOP), Ouro Preto, Minas Gerais, Brazil.
Int J Toxicol. 2015 May-Jun;34(3):250-7. doi: 10.1177/1091581815580172. Epub 2015 Apr 13.
Chloroform is an organic solvent used as an intermediate in the synthesis of various fluorocarbons. Despite its widespread use in industry and agriculture, exposure to chloroform can cause illnesses such as cancer, especially in the liver and kidneys. The aim of the study was to analyze the effects of chloroform on redox imbalance and pulmonary inflammatory response in adult C57BL/6 mice. Forty animals were divided into 4 groups (N = 10): female (FCG) and male (MCG) controls, and females (FEG) and males (MEG) exposed to chloroform (7.0 ppm) 3 times/d for 20 minutes for 5 days. Total and differential cell counts, oxidative damage analysis, and protein carbonyl and antioxidant enzyme catalase (CAT) activity measurements were performed. Morphometric analyses included alveolar area (Aa) and volume density of alveolar septa (Vv) measurements. Compared to FCG and MCG, inflammatory cell influx, oxidative damage to lipids and proteins, and CAT activity were higher in FEG and MEG, respectively. Oxidative damage and enzyme CAT activity were higher in FEG than in FCG. The Aa was higher in FEG and MEG than in FCG and MCG, respectively. The Vv was lower in FEG and MEG than in FCG and MCG, respectively. This study highlights the risks of occupational chloroform exposure at low concentrations and the intensity of oxidative damage related to gender. The results validate a model of acute exposure that provides cellular and biochemical data through short-term exposure to chloroform.
氯仿是一种有机溶剂，用作各种碳氟化合物合成的中间体。尽管它在工农业中广泛使用，但接触氯仿会引发癌症等疾病，尤其是在肝脏和肾脏。本研究的目的是分析氯仿对成年C57BL/6小鼠氧化还原失衡和肺部炎症反应的影响。40只动物分为4组（每组10只）：雌性（FCG）和雄性（MCG）对照组，以及雌性（FEG）和雄性（MEG），每天3次暴露于氯仿（7.0 ppm），每次20分钟，持续5天。进行了总细胞和分类细胞计数、氧化损伤分析以及蛋白质羰基和抗氧化酶过氧化氢酶（CAT）活性测量。形态计量分析包括肺泡面积（Aa）和肺泡隔体积密度（Vv）测量。与FCG和MCG相比，FEG和MEG中的炎症细胞浸润、脂质和蛋白质的氧化损伤以及CAT活性分别更高。FEG中的氧化损伤和酶CAT活性高于FCG。FEG和MEG中的Aa分别高于FCG和MCG。FEG和MEG中的Vv分别低于FCG和MCG。本研究强调了低浓度职业性接触氯仿的风险以及与性别相关的氧化损伤强度。研究结果验证了一种急性暴露模型，该模型通过短期接触氯仿提供细胞和生化数据。
