title: Pycnogenol prevents potassium dichromate K2Cr2O7-induced oxidative damage and nephrotoxicity in rats.
abstract: Environmental and occupational exposure to chromium compounds, especially hexavalent chromium [Cr(VI)], is widely recognized as a potential nephrotoxic in humans and animals. Its toxicity is associated with overproduction of free radicals, which induces oxidative damage. Recent evidence indicates that Pycnogenol (PYC), French maritime pine bark extract, exhibits antioxidant potential and protects against various oxidative stressors. The aim of the present study was to examine the modulating impacts of PYC on potassium dichromate K2Cr2O7-induced oxidative damage and nephrotoxicity in rats. Male Wistar rats were divided into four groups. The first group was control, the second group was control plus pre-treated with PYC (10 mg/kg, body weight; in saline; intraperitoneally; once daily for 3 weeks) as drug control and the third group was saline pre-treated plus treated with a single injection of K2Cr2O7 (15 mg/kg, body weight; in saline; intraperitoneally) as toxicant group. The fourth group was PYC pre-treated plus K2Cr2O7 injected. Forty-eight hours after K2Cr2O7-treatment, blood was drawn for estimation of renal injury markers in serum. Rats were then sacrificed, and their kidneys were dissected for biochemical and histopathological assays. K2Cr2O7-treated rats showed significant increases in markers of renal injury in serum, including blood urea nitrogen (BUN), serum creatinine (Scr), and alkaline phosphatase (ALP), which were significantly (P < 0.05) decreased by PYC pre-treatment. Moreover, prophylactic pre-treatment of rats with PYC significantly (P < 0.05) ameliorated increased thiobarbituric reactive substances (TBARS), malonaldehyde (MDA) and protein carbonyl (PC), and decreased levels of glutathione (GSH) and catalase activity in the kidney homogenate of K2Cr2O7-treated rats. These results were also supported and confirmed with histopathological findings. The study suggests that PYC is effective in preventing K2Cr2O7-induced oxidative mediated nephrotoxicity, but more studies are needed to confirm the effects of PYC as a nephroprotective agent.
authors: Department of Biochemistry, Lipid Metabolism Laboratory, Jamia Hamdard (Hamdard University), New Delhi 110062, India.
authors: Kehkashan
authors: K
authors: Parveen
authors: Mohd Rashid
authors: MR
authors: Khan
authors: Waseem A
authors: WA
authors: Siddiqui
mesh_terms: D000818:Animals; D002374:Catalase / Q000378:metabolism; D005419:Flavonoids / Q000494:pharmacology*; D005978:Glutathione / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000473:pathology / Q000502:physiology; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D010936:Plant Extracts; D011192:Potassium Dichromate / Q000037:antagonists & inhibitors* / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D005419:Flavonoids; D010936:Plant Extracts; C024070:pycnogenols; D002374:Catalase; D005978:Glutathione; D011192:Potassium Dichromate