The para isomer of dinitrobenzene disrupts redox homeostasis in liver and kidney of male wistar rats

Janet Olayemi Sangodele; Mary Tolulope Olaleye; Thomas K Monsees; Afolabi Clement Akinmoladun

doi:10.1016/j.bbrep.2017.04.017

The para isomer of dinitrobenzene disrupts redox homeostasis in liver and kidney of male wistar rats

Biochem Biophys Rep. 2017 May 4:10:297-302. doi: 10.1016/j.bbrep.2017.04.017. eCollection 2017 Jul.

Authors

Janet Olayemi Sangodele^{1

2}, Mary Tolulope Olaleye¹, Thomas K Monsees², Afolabi Clement Akinmoladun¹

Affiliations

¹ Phytomedicine, Biochemical Pharmacology and Toxicology Laboratories, Department of Biochemistry, School of Sciences, PMB 704, The Federal University of Technology, Zip code: 340001, Akure, Nigeria.
² Department of Medical Biosciences, 4th floor, Life Science Building, Faculty of Natural Science, University of the Western Cape, Bellville, Cape Town, South Africa.

Abstract

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.

Keywords: ALP, alanine phosphatase; CAT, Catalase; Environmental toxicants; GSH, glutathione; GST, glutathione –s –transferase, GPX, glutathione reductase, NIH, national institute of health; H&E, hamatoxilin eosin; Kidney; LPO, lipid peroxidation; Liver; MDA, malodialdehyde; OECD, Organisation for economic co-operation and Development; Oxidative stress; PHS, public health service; SOD, Superoxide dismutase; SPSS, Statistical Pucteage for Social Sciences; Sub-dermal; TBA, thiobarbituric acid; TNB, trinitrobenzene; o-DNB, ortho-dinitrobenzene, m-DNB, meta-dinitrobenzene; p-DNB, para-dinitrobenzene; p‐DNB.