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1.
The World Journal of Men's Health ; : 141-149, 2013.
Article in English | WPRIM | ID: wpr-172358

ABSTRACT

PURPOSE: The purpose of the present study was to investigate the effect of sesame oil on the reproductive parameters of diabetic male Wistar rats. MATERIALS AND METHODS: The adult male rats in a split plot design were divided into normal (n=10), normal 5% (n=5; 5% sesame oil enriched diet), diabetic (Streptozocin induced diabetes; n=9), diabetic 5% (n=9; 5% sesame oil enriched diet), and diabetic 10% (n=9; 10% sesame oil enriched diet) groups. Diet supplementation continued for 56 days. RESULTS: Sesame oil supplementation did not reduce the plasma glucose concentration of rats in the diabetic groups (p>0.05). The total spermatogonia, spermatocytes, Leydig cells/tubule, and the germ cell to Sertoli cell ratio were lower in the diabetic rats than the normal ones (p<0.05), and with the exception of spermatogonia counts, these values improved by the addition of sesame oil to the diet (p<0.05). The sperm progressive motility and viability were lower in the diabetic rats (p<0.05) and sesame oil supplementation did not improve them. Incorporation of sesame oil into the diet improved the plasma testosterone concentration of the diabetic rats in a dose-dependent manner (p<0.05). CONCLUSIONS: In summary, sesame oil supplementation improved the reproductive parameters of diabetic rats at the levels of the testicular microstructure and function, but was not effective in protecting the epididymal sperm.


Subject(s)
Adult , Animals , Male , Rats , Diabetes Mellitus , Diet , Germ Cells , Sesame Oil , Sesamum , Spermatocytes , Spermatogonia , Spermatozoa , Testis , Testosterone
2.
Archives of Iranian Medicine. 2012; 15 (11): 696-701
in English | IMEMR | ID: emr-160612

ABSTRACT

Cancer is the fifth leading cause of death worldwide. There are considerable efforts to identify naturally occurring substances for use as new drugs in cancer therapy. Some components of animal venoms have been identified that possess substantial anticancer properties. In our previous studies, the cytotoxic effects of ICD-85 [venom-derived peptides] have been reported on HL-60 and MDA-MB231 cell lines. This has prompted us to investigate the comparative cytotoxic effects of ICD-85 on the HeLa cell line and normal lamb kidney [LK] cells. Cells were exposed to various concentrations [8 x 10[4] to 5.6 x 10 microg/mI] of ICD-85 at various incubation times [24, 48 and 72 hours]. Cell viability was measured by the MTT assay. A morphological study was also carried out using an inverted microscope. Caspase-8 activity was assayed by the Caspase-8 Colorimetric Assay Kit in HeLa cells that were exposed to ICD-85 for 48 hours. Data analysis showed that ICD-85 has a dose-dependent cytotoxic effect on HeLa cells with an inhibitory concentration 50% [IC[50]] of 26.62 +/- 2.13 microg/mI at 24 hours, 27.33 +/- 2.35 microg/mI at 48 hours, and 28.13 +/- 2.52 microg/mI at 72 hours. Results also indicated that the cytotoxic effect of ICD-85, at 48 and 72 hours incubation times did not show significant alteration compared to 24 hours of exposure. Interestingly, the minimum concentration of ICD-85 which showed a cytotoxic effect on LK cells was found to be 3500-fold less than the minimum concentration that showed a cytotoxic effect on the HeLa cancer cells. While morphological analysis revealed a significant difference that included the characteristic rounding of dying cells by treatment with ICD-85 compared with untreated HeLa cells, this difference was not observed in normal cells. ICD-85 increased caspase-8 activity in HeLa cells after 48 hours of exposure. ICD-85 has a dose-dependent cytotoxic effect on HeLa cancer cells in contrast with its negligible effect on normal LK cells

3.
IJPR-Iranian Journal of Pharmaceutical Research. 2012; 11 (3): 931-938
in English | IMEMR | ID: emr-160882

ABSTRACT

Our previous studies revealed an inhibitory effect of ICD-85 [Venom derived peptides] on breast cancer cell line MDA-MB231. ICD-85 was also confirmed by in-vivo studies to suppress the breast tumor in mice. However, the exact mechanism of ICD-85 was unknown. Hence, the present study was undertaken to assess the mechanism of ICD-85 effect as an anti-proliferative agent of cancer cells. The effect of ICD-85 on proliferation of HL-60 cancer cells was determined by using the MTT assay. The morphological changes of ICD-85 treated HL-60 cells were observed under transmission electron microscope [TEM] DNA fragmentation analysis was also carried out using gel electrophoresis. ICD-85 induced the marked inhibition of HL60 cell proliferation with an IC[50]-value of 0.04 |ug/mL following 24 h of incubation. ICD-85 treated cells when compared with untreated cells, showed nuclear material condensation, endoplasmic reticulum dilation, mitochondria swelling or degradation, increased cytoplasmic vacuoles, reduction or disappearance in cytoplasmic process and decreased nuclear/cytoplasmic ratio was observed. The characteristic DNA ladder formation of ICD-85-treated cells in agarose gel electrophoresis confirmed the results obtained through the electron microscopy. The results of the present study indicated that ICD-85 inhibited the cancer cell proliferation by inducing cell apoptosis

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