Carvacrol attenuates cyclophosphamide-induced oxidative stress in rat kidney.
Cyclophosphamide (CP) is an antineoplastic drug that induces kidney damage via producing oxidative stress. Carvacrol (CAR) has antioxidative effect and we postulated that it can be protective against CP-induced nephrotoxicity. Six groups (n = 7) of rats (control, 100 mg/kg CP, CP+5 mg/kg CAR, CP+10 mg/kg CAR, 5 mg/kg CAR, and 10 mg/kg CAR) were injected intraperitoneally. Serum malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), creatinine (CRE), total antioxidant capacity (TAC), and total oxidant state (TOS) were measured, and oxidative stress indexes (OSI) were calculated. Kidneys were also analyzed histologically. In CP-alone group MDA, CRE, TOS, and OSI levels increased whereas GSH, SOD, CAT, and TAC levels decreased compared with control group. In CP plus CAR groups, MDA, TOS, and OSI levels decreased whereas GSH, SOD, CAT, and TAC levels increased compared with CP-alone group. However, CRE levels were similar in CP-alone and CP+5 CAR group whereas decreased in CP+10 CAR group. CP+10 CAR group was significantly different in all parameters (except TAC) from CP+5 CAR group. Kidney microscopy was showed lower tissue damage in CP plus CAR groups. In conclusion, 10 mg/kg CAR is more effective than 5 mg/kg CAR in prevention of CP-induced oxidative damage on kidney.
a Department of Biology, Faculty of Arts and Science, Eskisehir Osmangazi University, 26480 Eskisehir, Turkey.
Sibel
S
Gunes
a Department of Biology, Faculty of Arts and Science, Eskisehir Osmangazi University, 26480 Eskisehir, Turkey.
Adnan
A
Ayhanci
b Department of Histology and Embryology, Faculty of Medicine, Eskisehir Osmangazi University, 26480 Eskisehir, Turkey.
Varol
V
Sahinturk
c Department of Medical Biochemistry, Faculty of Medicine, Karadeniz Technical University, 61080 Trabzon, Turkey.
Diler Us
DU
Altay
d Department of Physiology, Faculty of Medicine, Eskisehir Osmangazi University, 26480 Eskisehir, Turkey.
Ruhi
R
Uyar
D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D015415:Biomarkers / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D003404:Creatinine / Q000378:metabolism; D003520:Cyclophosphamide / Q000009:adverse effects*; D000081007:Cymenes; D004305:Dose-Response Relationship, Drug; D005978:Glutathione / Q000378:metabolism; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D039821:Monoterpenes / Q000494:pharmacology*; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism
D000975:Antioxidants; D015415:Biomarkers; D000081007:Cymenes; D039821:Monoterpenes; D008315:Malondialdehyde; D003520:Cyclophosphamide; C073316:carvacrol; D003404:Creatinine; D002374:Catalase; D013482:Superoxide Dismutase; D005978:Glutathione
carvacrol; cyclophosphamide; cytoprotection; nephrotoxicity; néphrotoxicité; oxidative stress; stress oxydatif