Starovlah 2019b MiP2019
Mitochondria are key component of energy production, oxidative stress, calcium homeostasis, steroid biosynthesis, but also the key component of stress response. However, the molecular adaptation of spermatozoa from stressed males was not described well.
The aim of this study was to determine the functionality and molecular adaptation of spermatozoa from stressed rat by applying in vivo and in vitro approach. For in vivo experimental model, psychophysiological stress by immobilization (IMO), was performed for 3 hours in different time during the day (ZT3, ZT11, ZT23), for one (1xIMO) or ten (10xIMO) consecutive days. For in vitro approach, epididymal spermatozoa from undisturbed rats were stimulated with stress hormones adrenaline and cortisol.
Results showed that number of spermatozoa significantly decreased in all 10xIMO rats comparing to control. Acrosomal status (response to acrosome-reaction-inducer progesterone) significantly decreased in spermatozoa from 1xIMO and 10xIMO rats comparing to control. The same effect was observed in spermatozoa stimulated in vitro with stress hormones. RQ-PCR results revealed that transcription of the main mitochondrial biogenesis markers Ppargc1a, Nrf1 and Nrf2 increased in spermatozoa from 10xIMO rats in ZT3 time point. In the same spermatozoa samples transcription of main markers of mitochondrial architecture Opa1, Mfn1, Mfn2 increased in ZT3 while decreased in ZT11 time point. Incubation of spermatozoa with adrenaline decreased level of Ppargc1a and Nrf2a transcripts, while cortisol decreased expression of mitochondrial transcription factor TFAM.
In summary, repeated psychophysical stress decreased the number and functionality of spermatozoa and disturbed transcriptional profile of their mitochondrial biogenesis and architecture markers.
Labels: MiParea: mt-Biogenesis;mt-density, mtDNA;mt-genetics, nDNA;cell genetics, Comparative MiP;environmental MiP
Organism: Rat Tissue;cell: Genital
Affiliations and support
- Lab Reproductive Endocrinology Signaling, Lab Chronobiology Aging, Centre Excellence CeRES, Fac Sciences, Univ Novi Sad, Novi Sad, Serbia. - [email protected]
- This work was supported by the grant no. 173057 and grant no. 451-0302807 Centre of Excellence CeRES from the Ministry of Education, Science and Technological Development, Republic of Serbia, as well as grant no. 2130 from the Autonomous Province of Vojvodina.