The aim of the present study was to investigate the ameliorative effect of curcumin (CMN) against acute cadmium chloride (CdCl(2)) toxicity on male reproductive system in rats. CdCl(2) is known to be a heavy metal and potential environmental pollutant. For this purpose, 28 rats were equally divided into four groups; the first group was kept as control and given distilled water and corn oil as carrier. In second and third groups, CdCl(2) and CMN were administered at the dose with 1 mg kg(-1) day(-1) and 100 mg kg(-1) for 3 days respectively. CdCl(2) and CMN were given together at the same doses in the fourth group. It was determined that acute CdCl(2) exposure caused a significant reproductive damage via increased oxidative stress (increased TBARS levels and decreased SOD, CAT, GPx and GSH levels), histological alterations (necrosis, oedema etc.) and spermatological damage (decreased sperm motility and sperm concentration and increased abnormal sperm rate) in male rats. However, CMN treatment partially reversed these toxic effects of CdCl(2) on the reproductive system. In conclusion, our results show that acute exposure of CdCl(2) may lead to infertility, and CMN could prevent and reverse hazardous effects of CdCl(2) to some degree. Thus, CMN may be useful for the prevention of CdCl(2)-induced reproductive damage.

In the current study, the protective effect of montelukast (ML) on cisplatin induced reproductive toxicity in rats was investigated. Twenty-eight rats were equally divided into four groups; first group was kept as control. In the second group, ML was orally administered at the dose of 10 mg/kg/day for 10 days. In the third group, CP was intraperitoneally administered at the dose of 7 mg/kg a single injection, and in fourth group, CP and ML were given together at the same doses. Although CP induced oxidative stress via significant increase in the formation of TBARS, it caused a significant decline in the levels of GSH, CAT, GPx, and SOD in rats. In contrast, ML prevents these effects of CP through cause an increase in GSH, CAT, GPx, and SOD levels and a decrease in formation of TBARS. In addition, sperm motility and serum testosterone levels significantly decrease and histopathological damage increases with CP treatment. However, the effects of CP on sperm motility, serum testosterone level, oxidative and histopathological changes are eliminated by ML treatment. In conclusion, the current study demonstrated that the reproductive toxicity caused by CP may be prevented by ML treatment. Thus, it was judged that co-administration of ML with CP may be useful to attenuate the negative effects of CP on male reproductive system.

In this study, it was aimed to determinate beneficial effects of protocatechuic acid (PCA) against reproductive toxicity caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), an environmental contaminant. For this purpose, 28 rats were equally divided into four groups (control, TCDD 2 μg kg(-1) per week, PCA 100 mg kg(-1) per day and TCDD + PCA group), and compounds were orally administered for 45 days. The results indicated that TCDD induced oxidative stress via an increase in thiobarbituric acid-reactive substances levels and a decrease in reduced glutathione, catalase, glutathione peroxidise and SOD levels in male rats. In contrast, PCA treatment prevented toxic effects of TCDD in terms of oxidative stress. Additionally, sperm motility, sperm concentration and serum testosterone levels significantly decreased, and pathologic testicular damage increased with TCDD exposure. However, these effects of TCDD on sperm characteristics, histopathological changes and hormone levels were reversed by PCA treatment. In conclusion, it was found that TCDD exposure induced reproductive toxicity (oxidative, hormonal, histopathological and spermatological alternations) in male rats and PCA treatment could prevent toxic effects of TCDD. Thus, PCA may be useful for the prevention and treatment of reproductive toxicity caused by TCDD.

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