Over doses of Paracetamol (panadol; acetaminophen) can cause life-threatening renal damage. This study compared the impact of nano-ubiquinone (Nubiq) with native ubiquinone (ubiq) reducing damage induced by Paracetamol-toxicity in rats. Paracetamol treatment produced an elevation in serum urea, uric acid, creatinine, C-reactive protein, renal nitric oxide, and lipid peroxide levels, and reductions in interleukin-10, superoxide dismutase, and glutathione levels. Meanwhile, c-Jun N-terminal kinases, vascular cell adhesion protein-1, cyclooxygenase-2 protein, and kidney injury molecule-1 were highly expressed, and NFE2-related factor 2 gene expression was down-regulated. Destruction of the epithelium, necrosis, and inflammatory cell infiltration could be observed in the renal tissue. Treatment with both ubiq an nubiq significantly ameliorated all of these signs. These findings suggest that Nubiq achieved the most significant amelioration in oxidative stress and inflammatory biomarkers in paracetamol -induced nephrotoxicity.
Keywords: COX-2; DNA; JNK; KIM-1; NanoNubiquinone; VCAM.