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Showing 2 results for Feizollah

Mirfeizollahi A, Farivar Sh, Akhondi Mm, Modarresi Mh, Hodjat M, Sadeghi Mr,
Volume 66, Issue 12 (5 2009)
Abstract

Background: Pi-GST and Mu-GST are subclasses of glutathione S-transferase that present on human sperm surface and play an important role against oxidative stress. Therefore, any defects in the enzyme activity may be associated with male infertility.In this study the polymorphisms of GSTM1 and GSTP1 in association with enzyme activity and sperm parameters were studied.

Methods: This case-control study involved 95 men with oligoastenoteratozoospermia and 26 controls with normozoospermia. Semen analyses were carried out according to WHO guidelines. Blood DNA was extracted using salting out procedures. GSTM1 and GSTP1 polymorphisms gene were determined through PCR-RFLP and multiplex PCR, respectively. Finally, Glutathione S-transferase activity was measured.

Results: Frequencies of GSTM1 null genotype in oligoastenoteratospermic and normospermic groups were 52.1% and 53.8% respectively. There were no statistically significant differences in sperm parameters and enzyme activity between GSTM1 null and positive genotypes in two groups. There were no statistically significant differences in glutathione S-transferase activity between oligoastenoteratospermia and normospermic groups (p>0.05). All the 121 men in this study had Ile/Ile genotypes at 105 codon of GSTP1. Frequency of normal homozygote (114Ala/Ala), heterozygote (114Ala/Val) and mutant homozygote (114Val/Val) genotypes in oligoastenoteratospermic group were 81.1%, 17.9% and 1.1% respectively but in the control group they were 88.5%, 11.5% and null.

Conclusions: Total glutathione S-transferase activity and sperm parameters were not affected by deficient Glutathione S-transferase activity in GSTM1 null genotype. Compensate activity of other sperm surface glutathione S-transferase isozymes, like GSTP1, may justify the cause.


Sallahadin Feizollah , Shiva Khezri ,
Volume 73, Issue 8 (November 2015)
Abstract

Background: Multiple Sclerosis (MS) is a neurodegenerative disease of the central nervous system (CNS). The hippocampus is a vital center for learning and memory it is extremely vulnerable to neurodegenerative diseases. The male hormones could be neuroprotective for the CNS. The current study is an attempt to investigate the effect of testosterone on learning and spatial memory following the demyelination of CA1 area by the injection of ethidium bromide in the rats' hippocampus. Methods: This experimental study has been conducted on healthy rats in the faculty of science of the Urmia University from September 2013 to February 2015. For demyelination in all previously gonadectomized healthy rats, 3µl ethidium bromide was injected into the CA1 area of rats by stereotaxic surgery. In addition, the treatment groups received 1µl testosterone (6µg/µl) during a 20-day timeframe on a daily basis after demyelination by the ethidium bromide. The control groups had no drug injection. The process of the learning and spatial memory of the rats were closely monitored by the radial Maze. The demyelination and remyelination in the hippocampus were checked by the myelin-specific coloring (Luxol fast blue and Cresyl violet). Results: The histological results suggest that the testosterone is capable of minimizing the destructive impacts of ethidium bromide in the treatment group as well as enhancing the remyelination process. In the group treated by testosterone, the percentage of the pyknotic cells 20 days after demyelination induction, represented a significant reduction compared to that of ethidium bromide group (P=0.008). The behavioral studies analyses show that the amount of the food finding time in those groups received ethidium bromide was significantly longer than those of the control groups (P=0.001). Furthermore, the application of the testosterone in the treatment groups reduced the extent of demyelination while the memory impairment induced by the ethidium bromide was significantly improved (P=0.001). Conclusion: Testosterone can act as a neuroprotective factor that reduces the extent of demyelination and the number of pyknotic cells. It also may improve the learning and memory impairment induced by ethidium bromide.



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