Investigation of protective effect of ellagic acid in phthalates-induced reproductive damage.

Phthalates that people are exposed to every day are toxic carcinogenic chemicals with proven harmful effects on growth and reproduction. Ellagic acid (EA) is a polyphenol derivative known for its antioxidant properties. We hypothesized that the possible reproductive damage mechanism of phthalates is oxidative attack and ellagic acid could have a protective effect against radical forms in the body through its antioxidant properties. Thirty-two male rats were randomly divided into 4 groups, with 8 rats in each. Phthalate (DBP) was administered intraperitoneally and EA acid through gastric oral gavage (phthalate group 500 mg/kg/day DBP; EA group 2 mg/kg/day ellagic acid; the treatment group 500 mg/kg/day DBP and 2 mg/kg/day EA). The vehicle of DBP and EA, carboxymethyl cellulose was administered to control group. At the end of 4 weeks the testis tissue samples were taken under mild anesthesia. Tissue malondialdehyde, antioxidant parameters, sperm motility, sperm density and abnormal spermatozoon ratios were determined. Analysis was performed with One Way ANOVA test using SPSS 12.0 program. As a result; it has been shown that DBP causes oxidative damage by increasing the malondialdehyde level and decreasing antioxidant parameters, increased abnormal sperm rate and decreased sperm motility and concentration and histopathological damage so this damage is inhibited by the antioxidant activity of ellagic acid.

18ß-glycyrrhetinic acid attenuates global cerebral ischemia/reperfusion-induced cardiac damage in C57BL/J6 mice

Abstract The aim of the present study is to investigate the cardioprotective effects of 18ß-glycyrrhetinic acid (18ß -GA) against oxidative and histological damage caused by global cerebral ischemia/ reperfusion (I/R) in C57BL/J6 mice. All male mice (n:40) were randomly divided into four groups: (1) sham-operated (Sham), (2) I/R, (3) 18ß-GA, and (4) 18ß -GA+I/R. Ischemia was not applied to the sham and 18ß-GA groups. In the I/R group, the bilateral carotid arteries were clipped for 15 min to induce ischemia, and the mice were treated with the vehicle for 10 days. In the 18ß-GA group, the mice were given 18ß-GA (100 mg/kg) for 10 days following a median incision without carotid occlusion. In the 18ß-GA+I/R group, the ischemic procedure performed to the I/R model was applied to the animals and afterwards they were intraperitoneally (i.p.) treated with 18ß-GA (100 mg/kg) for 10 days. It was found that global cerebral I/R increased TBARS levels and decreased antioxidant parameters. The 18ß-GA treatment decreased the level of TBARS and increased GSH, GPx, CAT, SOD activities. Also, the control group cardiac tissue samples were observed to have a normal histological appearance with the Hematoxylin-Eosin staining method. Histopathological damage was observed in the heart tissue samples belonging to the I/R group. The 18ß-GA treatment ameliorates oxidative and histological injury in the heart tissue after global ischemia reperfusion, and may be a beneficial alternative treatment