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10.1016/j.bbrep.2017.04.017

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suck abstract from ncbi


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pmid28955757      Biochem+Biophys+Rep 2017 ; 10 (ä): 297-302
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  • The para isomer of dinitrobenzene disrupts redox homeostasis in liver and kidney of male wistar rats #MMPMID28955757
  • Sangodele JO; Olaleye MT; Monsees TK; Akinmoladun AC
  • Biochem Biophys Rep 2017[Jul]; 10 (ä): 297-302 PMID28955757show ga
  • Background: Para-Dinitrobenzene (p-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 p-DNB. This study evaluated the effect of sub-chronic exposure of rats to p-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 p-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, p-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, p-DNB caused a significant increase in plasma urea concentration and serum, liver and kidney ALP activities relative to control. In addition, p-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 p-DNB may produce hepato-nephrotoxicity through oxidative stress.
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