| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2572368 | Toxicology Reports | 2014 | 7 Pages |
•Lead acetate reduced the sperm cell concentration, increased sperm abnormalities and decreased the superoxide dismutase (SOD) and catalase activities in male rats.•Addition of cinnamon to lead acetate enhanced the viability of the spermatozoa, preserved the sperm cell concentration and improved the level of SOD and catalase activities.•The expression of androgen receptor was reduced in testis of lead treated rats associated with increased the level of caspase-3 expression.•Cinnamon exhibited protective effect on reproductive system by inhibiting lead acetate induced oxidative stress and excessive cell apoptosis.
The aim of this study was to investigate the protective effects of cinnamon on lead acetate induced reproductive toxicities in rats. Thirty-two male rats were randomly divided into 4 groups, 8 rats in each. Control rats received distilled water, while treated rats received lead acetate (30 mg/kg), cinnamon (250 mg/kg) and lead acetate and cinnamon (30 mg/kg and 250 mg/kg) for 60 days by gavage tube. In cinnamon treated rats, the relative weights of testes, epididymis, seminal and prostate glands were significantly (P < 0.05) increased compared with that in lead acetate treated rats. Sperm cell concentration and viability were significantly (P < 0.05) reduced, while sperm abnormalities were significantly (P < 0.05) increased in lead treated rats. The superoxide dismutase (SOD) and catalase activities were significantly reduced (P < 0.001) in lead acetate treated rats compared to the other groups, while the addition of cinnamon to lead acetate improved the level of SOD compared to the lead treated group. There was a marked reduction (P < 0.001) in the expression of androgen receptor and significant (P < 0.001) increase in the level of caspase-3 protein expression in the testis of lead treated rats. In conclusion, cinnamon exhibited protective effect on reproductive system by inhibiting lead acetate induced oxidative stress and excessive cell apoptosis.
