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1.
Clinical and Experimental Reproductive Medicine ; : 90-96, 2016.
Article in English | WPRIM | ID: wpr-56133

ABSTRACT

OBJECTIVE: Diabetes mellitus (DM) is known to cause many systemic complications as well as male infertility. Astaxanthin (ASTX) is a powerful antioxidant that is involved in a variety of biologically active processes, including those with anti-diabetes effects. The present study investigates the effect of ASTX on the spermatozoa function in streptozotocin (STZ)-induced diabetic rats. METHODS: We divided 30 adult rats into three groups (10 rats per group), with a control group that received corn oil mixed with chow. DM was induced by intra-peritoneal injection of STZ. Eight weeks after the STZ injection, half of the diabetic animals were used as diabetic controls, and the rest were treated with ASTX for 56 days. Then the parameters and chromatin integrity of the epididymal sperm were analyzed using chromomycin A3, toluidine blue (TB), and acridine orange (AO) staining. RESULTS: The count, viability, and motility of the epididymal sperm were decreased significantly in the STZ group in comparison with the control group (count and viability, p<0.001; motility, p<0.001;0.01). ASTX increased normal morphology and viable spermatozoa compared to the STZ group (morphology, p=0.001; viability, p<0.001;0.05). The percentage of abnormal chromatins in TB and AO staining was higher in the STZ group compared to the control group (p<0.001;0.001). The mean percentage of TB and AO positive spermatozoa in STZ rats was significantly lower in the STZ+ASTX group (TB, p=0.001; AO, p<0.001;0.05). CONCLUSION: This study observed that in vivo ASTX treatment partially attenuates some detrimental effect of diabetes. Conversely, ASTX improved sperm viability, normal morphology, and DNA integrity.


Subject(s)
Adult , Animals , Humans , Male , Rats , Acridine Orange , Chromatin , Chromomycin A3 , Corn Oil , Diabetes Mellitus , Dietary Supplements , DNA , Infertility, Male , Spermatozoa , Streptozocin , Tolonium Chloride
2.
Singapore medical journal ; : 573-579, 2015.
Article in English | WPRIM | ID: wpr-276754

ABSTRACT

<p><b>INTRODUCTION</b>The aim of this study was to determine the effect of a high-fat diet (HFD) on oocyte maturation and quality in a mouse model.</p><p><b>METHODS</b>Female BALB/c mice were allocated to one of the following groups: (a) control group (n = 40), which received a controlled diet; or (b) HFD group (n = 40), which received an HFD for 12 weeks. Sections of the ovary were examined histologically. The number of follicles and corpora lutea were counted. In vitro maturation and in vitro fertilisation (IVF) were assessed in germinal vesicle (GV) and metaphase II (MII) oocytes, respectively. The expression of bone morphogenetic protein 15 (BMP15) and leptin receptor genes in GV and MII oocytes was evaluated using reverse transcription real-time polymerase chain reactions.</p><p><b>RESULTS</b>In the HFD group, there was a decreased number of primordial and Graafian follicles, as well as corpora lutea (p < 0.05). The rate of oocyte development to the MII stage was also reduced (p < 0.001). Cumulus expansion was observed more frequently in the control group than the HFD group (p < 0.05). The IVF rate in the HFD group was lower than that in the control group (p < 0.05). In the HFD group, BMP15 and leptin receptor genes were upregulated in the GV stage (p > 0.05) and MII stage (p < 0.05), compared to the control group.</p><p><b>CONCLUSION</b>An HFD reduces folliculogenesis in the primordial and Graafian stages, in vitro maturation and in vitro fertilisation rates, as well as oocyte quality in mice.</p>


Subject(s)
Animals , Female , Mice , Body Weight , Bone Morphogenetic Protein 15 , Metabolism , Corpus Luteum , Pathology , Diet, High-Fat , Fertility , Fertilization in Vitro , Methods , Gene Expression Regulation , Metaphase , Mice, Inbred BALB C , Obesity , Oocytes , Cell Biology , Pathology , Ovarian Follicle , Pathology , Ovary , Metabolism , Pathology , Photography , Polymerase Chain Reaction , Receptors, Leptin , Metabolism
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