Title of article :
Protective effect of polydatin, a natural precursor of resveratrol, against cisplatin-induced toxicity in rats
Author/Authors :
Ince، نويسنده , , Sinan and Arslan Acaroz، نويسنده , , Damla and Neuwirth، نويسنده , , Ond?ej and Demirel، نويسنده , , Hasan Huseyin and Denk، نويسنده , , Baris and Kucukkurt، نويسنده , , Ismail and Turkmen، نويسنده , , Ruhi، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2014
Pages :
7
From page :
147
To page :
153
Abstract :
The aim of the present study was to evaluate the possible protective effect of polydatin (PD) on cisplatin (Cis) induced oxidative stress in rats. Totally, thirty male Wistar albino rats were fed standard rodent diet and divided into 5 equal groups: the control group (vehicle treated) was treated with physiological saline for ten days both orally and intraperitoneally (i.p.), the second group was orally treated with physiological saline and 7 mg/kg single i.p. injection of Cis on the seventh day, and third, fourth, and fifth groups were treated orally PD at 25, 50, and 100 mg/kg/day, respectively for 10 days starting seven days before Cis injection and 7 mg/kg single i.p. Cis was injected on the seventh day. Cis resulted in significant increase malondialdehyde levels and decreased glutathione levels. In addition, Cis treatment decreased superoxide dismutase and catalase activities in erythrocyte and tissues. Also, Cis treatment caused to increase DNA damage and affected serum biochemical parameters whereas slightly decreased AchE activity. However, treatment of PD resulted in reversal of Cis-induced oxidative stress, lipid peroxidation, and activities of antioxidant enzymes. In conclusion, PD has protective effect in rats against Cis-induced oxidative stress, enhances antioxidant defence mechanism, and regenerates their tissues.
Keywords :
TOXICITY , Rat , Cisplatin , Polydatin , oxidative stress , DNA damage
Journal title :
Food and Chemical Toxicology
Serial Year :
2014
Journal title :
Food and Chemical Toxicology
Record number :
2127091
Link To Document :
بازگشت