The Effect of 8-Weeks of Low-Intensity Swimming Training on Promyelocytic Leukemia Zinc Finger Protein and Spermatid Transition Nuclear Protein Gene Expression in Azoospermic Rats Model

Aims: One of the causes of infertility in men is the azoospermia disease, which is attributed to the lack of sperm in each sperm. The primary function of spermatogenesis is the maintenance, proliferation, and differentiation of spermatogonial cells. Thus, the present study aimed to investigate the changes in Promyelocytic Leukemia Zinc Finger (PLZF) and spermatid Transition Nuclear Protein (TNP) gene expression levels in an azoospermic rat model after 8 weeks of low-intensity aerobic training. Methods & Materials: In this experimental study, 15 adult male Wistar rats were randomly divided into three groups of healthy control, with azoospermia, and exercise plus azoospermia after creating an azoospermia model. The patient plus exercise group performed a low-intensity swimming exercise 30 minutes a day, five days a week for 8 weeks, after the creation of the azoospermic rats. A One-way ANOVA test was used for data analysis. Findings: The results showed that a period of swimming exercise program in the exercise plus azoospermia group significantly reduced PLZF gene expression compared to the healthy control groups (P=0.001) and no significant increase to the azoospermia group (P=0.06). There was also a significant decrease in TNP gene expression levels in the exercise plus azoospermia group compared to the healthy control group (P=0.001) and a significant increase in the azoospermia group (P=0.057). Conclusion: Based on these Findings, it can be stated that the alteration of key molecules or signaling pathways and expression of the PLZF and TNP genes in the spermatogenesis process may increase infertility, but regular aerobic exercise, such as low-intensity swimming, helps to control the effects of infertility by increasing the maintenance and development of spermatogonial stem cells.

Reactive Oxygen Species Regulate the Inflammatory Function of NKT Cells through Promyelocytic Leukemia Zinc Finger

Reactive oxygen species (ROS) are byproducts of aerobic metabolism and contribute to both physiological and pathological conditions as second messengers. ROS are essential for antigen specific activation of T cells, but little is known about what role ROS play in NKT cells. In the current study, we investigated the role of ROS in NKT cell function. We found that ROS levels are similar among CD4, CD8 and NKT cell subsets in the thymus. However, NKT cells, but neither CD4 nor CD8 T cells, showed dramatically increased ROS in the spleen and liver but not in adipose tissues. ROS in the peripheral NKT cells were primarily produced by NADPH oxidases not mitochondria. Accordingly, ROS-high NKT cells were susceptible to oxidative stress and underwent apoptotic cell death. Furthermore, ROS play an important role in regulating the inflammatory function of NKT cells because antioxidant treatment of NKT cells showed reduced frequencies of IFN-γ+ and IL-17+ cells. In line with this, freshly isolated ROS-high NKT cells had more NKT1 and NKT17 cells but less NKT2 than ROS-low cells. These characteristics are regulated by promyelocytic leukemia zinc finger (PLZF) as evidenced by low ROS in NKT cells from PLZF haplodeficient mice and also from adipose tissues that do not express PLZF. Conversely, ROS were highly elevated in CD4 T cells from mice ectopically expressing PLZF. Together, our study revealed for the first time that ROS regulate NKT cell functions through PLZF.