Protective effects of caffeic acid phenethyl ester, vitamin C, vitamin E and N-acetylcysteine on vancomycin-induced nephrotoxicity in rats.
The objective of this study was to compare the beneficial effects of caffeic acid phenethyl ester (CAPE), vitamin C, vitamin E and N-acetylcysteine on vancomycin-induced nephrotoxicity. Thirty rats were randomly devided into six groups: (i) control; (ii) vancomycin, 200 mg/kg administrated via intraperitoneal route; (iii) vancomycin plus CAPE-vancomycin with 10 micromol/kg CAPE; (iv) vancomycin plus vitamin C-vancomycin (intraperitoneally) with 200 mg/dl vitamin C in drinking water; (v) vancomycin plus vitamin E-vancomycin with 1000 mg/kg body weight vitamin E (intramuscularly); and (vi) vancomycin plus N-acetylcysteine-vancomycin with 10 mg/kg body weight (intraperitoneally) of N-acetylcysteine. Vancomycin treatments were started 1 day after the first administrations of these agents and continued for 7 days. At the end of the experiments, catalase activity was significantly decreased by vancomycin in kidney homogenates (P < 0.05). Vitamin E, vitamin C, N-acetylcysteine and CAPE administrations decreased the blood urea nitrogen levels increased by vancomycin, although significant differences were detected only in the vitamins E and C groups (P < 0.05). Increased renal malondialdehyde and nitric oxide levels by vancomycin were significantly suppressed by agents used in the study (P < 0.05). Histopathological examination demonstrated prominent damages in the vancomycin-treated group. Vitamin E was the most beneficial agent on vancomycin-induced tubular damage, followed by vitamin C, N-acetylcysteine and CAPE treatments, respectively. The data suggest that vitamin E, as well as vitamin C, N-acetylcysteine and CAPE, could be useful for reducing the detrimental effects on vancomycin-induced toxicity in kidneys.
Ocak
Sabahattin
S
Department of Infectious Diseases and Clinical Microbiology, Faculty of Medicine, Mustafa Kemal University, Antakya, Turkey. sabahattinocak@hotmail.com
Gorur
Sadik
S
Hakverdi
Sibel
S
Celik
Sefa
S
Erdogan
Suat
S
D000111:Acetylcysteine / Q000494:pharmacology*; D000818:Animals; D000900:Anti-Bacterial Agents / Q000633:toxicity; D000975:Antioxidants / Q000494:pharmacology; D001205:Ascorbic Acid / Q000494:pharmacology*; D001806:Blood Urea Nitrogen; D002109:Caffeic Acids / Q000494:pharmacology*; D002374:Catalase / Q000378:metabolism; D004195:Disease Models, Animal; D004326:Drinking; D004338:Drug Combinations; D007273:Injections, Intramuscular; D007274:Injections, Intraperitoneal; D007668:Kidney / Q000187:drug effects / Q000201:enzymology / Q000473:pathology; D007674:Kidney Diseases / Q000139:chemically induced / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D010626:Phenylethyl Alcohol / Q000031:analogs & derivatives* / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D014640:Vancomycin / Q000633:toxicity*; D014810:Vitamin E / Q000494:pharmacology*; D014881:Water Supply
D000900:Anti-Bacterial Agents; D000975:Antioxidants; D002109:Caffeic Acids; D004338:Drug Combinations; D014810:Vitamin E; D014640:Vancomycin; D002374:Catalase; C055494:caffeic acid phenethyl ester; D010626:Phenylethyl Alcohol; D001205:Ascorbic Acid; D000111:Acetylcysteine