摘要
目的探讨长期低剂量双酚A(BPA)暴露对雄性大鼠肝脏的影响。方法将50只8周龄雄性Wistar大鼠随机分为普通对照组、高脂对照组、高脂饲料+低剂量BPA[10μg/(kg·d)]组、高脂饲料+中剂量BPA[50μg/(kg·d)]组和高脂饲料+高剂量BPA[250μg/(kg·d)]组,共5组。连续35周通过饮食途径给予大鼠BPA后,测定体质量、肝脏系数、体脂百分数,肝脏中甘油三酯、总胆固醇、丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)以及肝脏丙二醛(MDA)和谷胱甘肽过氧化物酶(GSH-Px)指标。结果高脂饲料组与普通饲料组血清中AST水平无差别,但高脂饲料组的血清中ALT水平明显高于普通饲料组(P<0.01);此外,高脂饮食+高剂量BPA组大鼠血清中AST和ALT水平均明显高于高脂饲料组(P<0.05),不同剂量的BPA对大鼠体质量、体脂百分数、肝脏中脂肪及MDA和GSH-Px均无明显影响(P>0.05)。结论长期高剂量BPA暴露对高脂喂养雄性大鼠肝脏功能具有明显的损害作用。
Objective To study the effects of long-term and low-dose of bisphenol A(BPA)on liver in male rats fed with high-fat diet. Methods Fifty 8-week old male Wistar rats were randomly divided into a standard chow diet group (STD), high-fat diet group (HFD), and high-fat diet plus low-dose of BPA (10μg/kg/day)group, high-fat diet plus middle-dose of BPA (50 μg/kg/day)group, high-fat diet plus high- dose of BPA (250 μg/kg/day)group. After 35-week treatment, the body weight, liver coefficient and body- fat percentage, total triglycerides(TG), total cholesterol(TC)of liver, alanine aminotransferase(ALT)and aspartic transaminase(AST) in serum, and malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) in liver were determined. Results There was no difference of serum AST level between STD and HFD0 but the serum ALT level of HFD group was higher than STD group(P〈0.01). Moreover, the serum AST and ALT levels of HFI)-BPA (250 μg/kg/day)were significantly higher than HFD group (P〈0.05); and the body weight, body-fat percentage, hepatic lipid, and MDA and GSH-Px levels of liver in rats were not significantly affected by different doses of BPA treatment(P〉0.05). Conclusions Long-term and high-dose of BPA treatment has a significant effect on liver function in high-fat diet fed male rats.
作者
丁世彬
李红玉
范瑛
应晨江
DING Shi-bin LI Hong-yu FAN Ying YING Chen-jiang(School of Public Health, Xinxiang Medical University, Xinxiang 453003 Chin)
出处
《工业卫生与职业病》
CAS
2017年第4期288-291,共4页
Industrial Health and Occupational Diseases
基金
国家自然科学基金资助项目(81172674)
关键词
双酚A
肝脏
脂代谢
氧化损伤
Bisphenol A
Liver
Lipid metabolism
Oxidative damage