二硝基苯的对位异构体破坏雄性Wistar大鼠肝脏和肾脏中的氧化还原稳态。
The para isomer of dinitrobenzene disrupts redox homeostasis in liver and kidney of male wistar rats.
作者信息
Sangodele Janet Olayemi, Olaleye Mary Tolulope, Monsees Thomas K, Akinmoladun Afolabi Clement
机构信息
Phytomedicine, Biochemical Pharmacology and Toxicology Laboratories, Department of Biochemistry, School of Sciences, PMB 704, The Federal University of Technology, Zip code: 340001, Akure, Nigeria.
Department of Medical Biosciences, 4th floor, Life Science Building, Faculty of Natural Science, University of the Western Cape, Bellville, Cape Town, South Africa.
出版信息
Biochem Biophys Rep. 2017 May 4;10:297-302. doi: 10.1016/j.bbrep.2017.04.017. eCollection 2017 Jul.
BACKGROUND
ParaDinitrobenzene -DNB) is one of the isomers of dinitrobenzene which have been detected as environmental toxicants. Skin irritation and organ toxicities are likely for industrial workers exposed to -DNB. This study evaluated the effect of sub-chronic exposure of rats to -DNB on cellular redox balance, hepatic and renal integrity.
METHODS
Forty eight male Wistar rats weighing 160-180 g were administered 50, 75, 1000 and 2000 mg/kg b.wt (body weight) of -DNB or an equivalent volume of vehicle (control) orally and topically for 14 days. After the period of treatment, the activities of kidney and liver catalase (CAT), alkaline phosphatase (ALP) and superoxide dismutase (SOD) as well as extent of renal and hepatic lipid peroxidation (LPO) were determined. Serum ALP activity and plasma urea concentration were also evaluated.
RESULTS
Compared with control animals, -DNB -administered rats showed decrease in the body and relative kidney and liver weights as well as increased renal and hepatic hydrogen peroxide and lipid peroxidation levels accompanied by decreased superoxide dismutase and catalase activities. However, -DNB caused a significant increase in plasma urea concentration and serum, liver and kidney ALP activities relative to control. In addition, -DNB caused periportal infiltration, severe macro vesicular steatosis and hepatic necrosis in the liver.
CONCLUSIONS
Our findings show that sub-chronic oral and sub-dermal administration of -DNB may produce hepato-nephrotoxicity through oxidative stress.
背景
对二硝基苯（-DNB）是已被检测出的环境毒物二硝基苯的异构体之一。接触-DNB的产业工人可能会出现皮肤刺激和器官毒性。本研究评估了大鼠亚慢性接触-DNB对细胞氧化还原平衡、肝脏和肾脏完整性的影响。
方法
将48只体重为160 - 180克的雄性Wistar大鼠，以50、75、1000和2000毫克/千克体重的剂量口服和局部给予-DNB或等量的赋形剂（对照），持续14天。治疗期结束后，测定肾脏和肝脏过氧化氢酶（CAT）、碱性磷酸酶（ALP）和超氧化物歧化酶（SOD）的活性以及肾脏和肝脏脂质过氧化（LPO）的程度。还评估了血清ALP活性和血浆尿素浓度。
结果
与对照动物相比，给予-DNB的大鼠体重、相对肾脏和肝脏重量降低，肾脏和肝脏过氧化氢及脂质过氧化水平升高，同时超氧化物歧化酶和过氧化氢酶活性降低。然而，与对照相比，-DNB使血浆尿素浓度以及血清、肝脏和肾脏ALP活性显著增加。此外，-DNB导致肝脏门周浸润、严重的大泡性脂肪变性和肝坏死。
结论
我们的研究结果表明亚慢性口服和皮下给予-DNB可能通过氧化应激产生肝肾毒性。
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