In recent years, cancer rates have been rising among reproductive-age women. Thus, chemotherapy exposure has become an important cause of premature ovarian failure (POF). There has been growing interest regarding the preservation and restoration of ovarian function before and after oncological treatment because of the reproductive risk of chemotherapeutics and improved long-term survival of cancer patients. In this study, we sought to analyze the effects of curcumin (CRC) and capsaicin (CPS) on cyclophosphamide-induced POF in a rat model. POF in rats was induced by intraperitoneal injection of 200 mg/kg cyclophosphamide on day 1 and then 8 mg/kg/day for the following 14 days. After 14 days of cyclophosphamide administration, rats were randomly divided into three groups as follows (n = 10/group): POF, POF + CRC (100 mg/kg/day), and POF + CPS (0.5 mg/kg/day) to determine the effects of CRC and CPS on the cyclophosphamide-induced POF rat model. Biochemical, hormonal, and histopathological evaluations were performed on blood and tissue samples 14 days after the CRC and CPS treatments. Malonaldehyde levels were significantly reduced, and glutathione levels and superoxide dismutase activity were significantly increased, in ovarian tissues in the POF + CRC and POF + CPS groups compared with the POF group. In the POF group, we observed hemorrhage and prominent mononuclear cell infiltration beneath the germinative epithelium, vascular congestion in ovarian stroma, hemorrhage around the corpus luteum, and atresia in ovarian follicles. This histopathological damage was significantly improved by treatment with CRC and CPS. There was a significant reduction in serum follicle-stimulating hormone and luteinizing hormone levels in rats treated with CRC and CPS compared with the POF group. Moreover, the levels of estradiol and anti-mullerian hormone in rats treated with CRC and CPS were significantly increased compared with the control group. In conclusion, CRC and CPS treatment of rats with cyclophosphamide-induced POF had a beneficial effect on reducing ovarian damage by improving tissue oxidative stress marker levels, ovarian reserve marker levels, and histopathological parameters. The significant improvements in ovarian tissue histopathological damage and hormonal levels detected in this study indicate that treatment with CRC or CPS might be a conservative treatment approach for cyclophosphamide-induced POF.

Thioacetamide (TAA) is an organosulfur, white crystalline compound having liver injury. However, it shows toxic effects on many organs. The reverts the oxidative stress created by TAA on the heart and kidney, and decreased lipid peroxide peroxidation back with antioxidant-properties nerolidol (NRL). This study hypothesized that NRL treatment a potential ameliorate nephrotoxicity and cardiotoxicity caused by TAA. Thirty-two Wistar Albino male rats (3-4 months old and 280-300 g in weight) were divided into four groups. (a) Control, (b) TAA was administered 200 mg/kg i.p. twice a weekly (c) NRL was orally administered at the dose of 100 mg/kg per every other day by gavages. (d) TAA and NRL-treated groups were assigned 200 mg/kg TAA and 100 mg/kg NRL for three weeks. As a result of these dose administration thiobarbituric acid reactive substances (TBARS) levels, superoxide dismutase (SOD), catalase (CAT), glutathione (GSH), and glutathione peroxidase (GPx) levels were detected. The results were shown that TAA leads to a significant rise in TBARS level and a significant decrease in GPx, CAT, SOD, and GSH levels in the heart and kidney tissue according to the control group. The finding of this study the NRL treatment reduced TBARS levels and increased antioxidant level. Administration of NRL prevents the biochemical and histopathological alterations induced by TAA. The findings of this study show that the antioxidant activity of NRL can protect against biochemical and histological damage caused by TAA in heart and kidney tissue.

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.

Objectives: Cisplatin is a powerful chemotherapeutic drug that is used to treatment a wide variety of cancers. Despite clinical data demonstrating the cardiotoxic effect of cisplatin, few studies have been carried to improve the cardiotoxicity of cisplatin. In cisplatin-induced toxicity, oxidative stress plays a critical role. This study determined the effect of Diospyros lotus L. fruit (DL), a powerful antioxidant plant, on heart damage caused by cisplatin through histological examination and oxidative stress parameters. Materials and Methods: Twenty eight male rats were randomly divided into four groups. An isotonic solution was given to the control group. A single dose of 7 mg/kg cisplatin was administered intraperitoneally to the cisplatin group. 1.000 mg/kg DL was given by gavage for 10 days to the DL group. Cisplatin and DL were administered together in the same doses to the treatment group. Thiobarbituric acid reactive substances (TBARS) levels, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities, and total glutathione (GSH) level were measured in the heart tissue of the experimental rats. Histological examination was also performed to determine any damage to the hearts of the experimental rats. Results: While TBARS levels in the cisplatin group increased significantly, SOD, CAT, GPx activities, and total GSH level decreased significantly. TBARS levels decreased significantly and SOD, CAT, GPx activities and GSH levels increased with DL treatment. According to the histological examination, histopathological differences were observed in the cisplatin group. Histopathological findings were either absent or decreased in the DL-treated group. Conclusion: Results of the study showed that DL therapy reduced oxidative stress and histological changes caused by cisplatin. DL could be a potential candidate for reducing cardiac damage caused by cisplatin.

The present study aimed to investigate the protective role of capsaicin in a rat model of 2,3,7,8-tetracholorodibenzo-p-dioxin (TCDD)-induced toxicity. Exposure to TCDD which is an environmental toxicant causes severe toxic effects in the animal and human tissues. Therefore, the potential protective effect of capsaicin in TCDD-induced organ damage was investigated in rats by measuring thiobarbituric acid reactive substances (TBARS) level, superoxide dismutase (SOD) activity, and glutathione (GSH) level in the heart, liver, and kidney tissues for oxidant/antioxidant balance. Thirty-two healthy adults (250–300 g weight and 3–4 months old) male Wistar albino rats were randomly distributed into four equal groups (n = 8): Control, CAP, TCDD, TCDD + CAP. A dose of 2 μg/kg TCDD or a dose of 25 mg/kg capsaicin were dissolved in corn oil and orally administered to the rats for 30 days. The results indicated that TCDD-induced oxidative stress by increasing the level of TBARS and by decreasing the levels of GSH, and SOD activity in the tissues of rats. However, capsaicin treatment was significantly decreased TBARS levels and was significantly increased GSH level and SOD activity (p < 0.05). In addition, capsaicin (25 mg/kg) significantly attenuated TCDD-induced histopathological alteration associated with oxidative stress in the heart, liver, and kidney tissues (p < 0.05). As capsaicin regulates oxidative imbalance and attenuates histopathological alterations in the rat tissues, it may be preventing agents in TCDD toxicity.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a common environmental contaminant that is toxic to brain, heart, kidney and liver. TCDD toxicity is due to free radical formation. Beta-glucan is an antioxidant that exhibits beneficial effects on health. We investigated the effects of beta-glucan on brain and liver tissues of rats with TCDD induced toxicity. We used female rats divided into four groups: control, TCDD group treated with TCDD 2 µg/kg/week, beta-glucan group treated with 50 mg/kg/day beta-glucan for 3 weeks, TCDD + beta-glucan group treated with 2 µg/kg/week TCDD and 50 mg/kg/day beta-glucan together for 3 weeks. We found that the thiobarbituric acid reactive substance (TBARS) levels were increased significantly in the TCDD group compared to the other groups. Glutathione (GSH) levels, and superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities were reduced in the TCDD group compared to the control group. SOD, CAT, GPx activities and GSH levels were increased in the TCDD + beta-glucan group. Histopathological observations were consistent with our biochemical findings. The oxidative stress and histopathology caused by TCDD were ameliorated by beta-glucan treatment. Beta-glucan should be explored for preventing brain and liver damage caused by TCDD toxicity.