Liu Jing, Qiao Shanlei, Ding Lu, Wang Shouyu, Cao Jinglian, Zhong Li, Liu Yang, Ni Chunhui, Zhu Baoli
The School of Public Health, Nanjing Medical University, Nanjing 211166, China.
E-mail:
Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi. 2015 Jul;33(7):538-40.
To study the influences of carbon disulfide (CS2) exposure on fatty acid metabolism in apolipoprotein E (ApoE) knockout mice and C57BL/6J mice.
Twenty-four male ApoE knockout mice were randomly and equally divided into four groups: a CS2-exposed normal diet group, a CS2-unexposed normal diet group, a CS2-exposed high-fat diet group, and a CS2-unexposed high-fat diet group. Twenty-four C57BL/6J male mice were divided into four groups in the same way. The CS2-exposed groups were exposed to CS2 (1 g/m(3)) by static inhalation for 5 hours a day, 5 days a week. After two weeks, the whole blood of mice was collected. Methyl ester derivatization of fatty acids was performed using an acid-catalyzed method. Fatty acid contents before and after exposure were compared by gas chromatography-mass spectroscopy.
There were significant differences in fatty acid contents of mice between the four groups. For the C57BL/6J mice, the arachidic acid contents in the CS2-exposed high-fat diet group were significantly lower than those in the CS2-unexposed high-fat diet group (P = 0.045 0). For the ApoE knockout mice, the arachidonic acid contents in the CS2-exposed normal diet group were significantly lower than those in the CS2-unexposed control diet group (P = 0.045 2). For the ApoE knockout mice, the γ-linolenic acid contents in the CS2-exposed high-fat diet group were significantly higher than those in the unexposed high-fat diet group (P = 0.044 7).
Exposure to CS2 can induce fatty acid metabolism disorder in mice, indicating that CS2 may increase the risk of atherosclerosis and other cardiovascular diseases.
研究二硫化碳(CS2)暴露对载脂蛋白E(ApoE)基因敲除小鼠和C57BL/6J小鼠脂肪酸代谢的影响。
将24只雄性ApoE基因敲除小鼠随机等分为四组:CS2暴露正常饮食组、未暴露于CS2的正常饮食组、CS2暴露高脂饮食组和未暴露于CS2的高脂饮食组。24只C57BL/6J雄性小鼠以同样的方式分为四组。CS2暴露组每天通过静态吸入暴露于CS2(1 g/m³),每周5天,共5小时。两周后,采集小鼠全血。采用酸催化法对脂肪酸进行甲酯衍生化。通过气相色谱-质谱联用仪比较暴露前后脂肪酸含量。
四组小鼠的脂肪酸含量存在显著差异。对于C57BL/6J小鼠,CS2暴露高脂饮食组的花生酸含量显著低于未暴露于CS2的高脂饮食组(P = 0.045 0)。对于ApoE基因敲除小鼠,CS2暴露正常饮食组的花生四烯酸含量显著低于未暴露于CS2的对照饮食组(P = 0.045 2)。对于ApoE基因敲除小鼠,CS2暴露高脂饮食组的γ-亚麻酸含量显著高于未暴露的高脂饮食组(P = 0.044 7)。
暴露于CS2可诱导小鼠脂肪酸代谢紊乱,表明CS2可能增加动脉粥样硬化和其他心血管疾病的风险。