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Showing 2 results for Abbasi Sarcheshmeh

Marzieh Rahimipour, Ali Reza Talebi, Morteza Anvari, Abolghasem Abbasi Sarcheshmeh, Marjan Omidi,
Volume 12, Issue 5 (6-2014)
Abstract


 
Background: Saccharin is an artificial non-caloric sweetener that used to sweeten products such as drinks, candies, medicines, and toothpaste, but our bodies cannot metabolize it. Sodium saccharin is considered as an important factor in tumor promotion in male rats but not in humans.
Objective: The objective of this study was to investigate the effect of saccharin consumption on sperm parameters and apoptosis in adult mice.
Materials and Methods: Totally 14 adult male mice were divided into 2 groups. Group 1 served as control fed on basal diet and group 2 or experimental animals received distilled water containing saccharin (0.2% w/v) for 35 days. After that, the left cauda epididymis of each mouse was cut and placed in Ham’s F10. Swimmed-out spermatozoa were used to analyze count, motility, morphology (Pap-staining) and viability (eosin-Y staining). Sperm DNA integrity, as an indicator of apoptosis, was assessed by SCD (sperm chromatin dispersion) and terminal deoxynucleotidyl transferase (TUNEL) assay.
Results: Following saccharin consumption, we had a reduction in sperm motility with respect to control animals (p=0.000). In addition, the sperm count diminished (17.70±1.11 in controls vs. 12.80±2.79 in case group, p=0.003) and the rate of sperm normal morphology decreased from 77.00±6.40 in control animals into 63.85±6.81 in saccharin-treated mice (p=0.001). Also, we saw a statistically significant increase in rates of sperm DNA damage and apoptosis in experimental group when compared to control one (p=0.001, p=0.002 respectively).
Conclusion: Saccharin consumption may have negative effects on sperm parameters, and increases the rate of sperm DNA fragmentation and apoptosis in mice.

Khadijeh Mirzaei Khorramabadi, Ali Reza Talebi, Abolghasem Abbasi Sarcheshmeh, Aghdas Mirjalili,
Volume 17, Issue 2 (February 2019 2019)
Abstract

Background: Generation of free radicals and oxidative stress are a major contributor to diabetes. These factors lead to the development of diabetic testicles disorders.
Objective: In this study, the protective effect of vitamin E on functional disorders associated with diabetes induced oxidative stress in male reproductive systems has been investigated.
Materials and Methods: Thirty-three adult male Mice were divided into control, diabetic, and untreated diabetic groups. Streptozotocin was used to induce diabetes. In the treated group, vitamin E was given to the Mice intraperitoneally for 30 days. Then, animals were anesthetized and sacrificed. Animal testicles were isolated and homogenized in phosphate buffer and used for measuring sperm count, motility and survival of sperm, MDA concentration and antioxidant capacity (TAC). Apoptosis was also performed with the TUNEL test.
Results: The results of reduction (12.03±98.11) TAC, MDA concentration (–28.5±2.58), sperm motility (unstable sperma= 86.4±7.48), sperm count (171.51), Sperm morphology (natural morphology= 49.69±31.93) and abnormal morphology (9.77±49.7) with increased oxidative damage. These changes were statistically significant in comparison with the control group for all variables other than MDA (p= 0.05). Treatment of vitamin E diabetic Mice improved the ability of antioxidants to prevent oxidativedamage in the testicles, restore the sperm movement, and increase the number of normal sperm as well as TAC. The level of apoptosis in the treated group has decreased compared to the untreated group.
Conclusion: Vitamin E protects the reproductive system against diabetes mellitus. Therefore, it was concluded that vitamin E may be a suitable agent for protecting the sperm and testicular parameters against undesirable effects of diabetes.
 

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