Molecular hydrogen may enhance the production of testosterone hormone in male infertility through hormone signal modulation and redox balance

Rahima Begum, Johny Bajgai, Ailyn Fadriquela, Cheol Su Kim, Soo Ki Kim, Kyu Jae Lee

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)


Since the discovery of molecular hydrogen (H 2 ) as a selective scavenger of free radicals like reactive oxygen species (ROS) and reactive nitrogen species (RNS), numerous studies have proved the potential application of H 2 in therapeutic and preventative medicine. Moreover, H 2 can regulate the intracellular signal as a signal modulator. However, it is still unclear in cell signaling involved in testosterone hormone production. Male fertility depends on the intra-testicular testosterone concentration, which is produced by the Leydig cell in the seminiferous tubules in testes. Although moderate amounts of ROS are needed for normal sperm function, the higher amounts might decrease testosterone production. High ROS decreases testosterone hormone production by dysregulation of hormonal signal from the hypothalamus to the Leydig cell as a result of redox imbalance. Lower level of testosterone fails to support the Leydig cell for the progression of spermatogenesis. Superoxide anion (O 2 [rad]− ), hydroxyl radical ( [rad] OH) and peroxynitrite (ONOO ) could also attack the DNA, lipid and protein, disrupting sperm structure and function and aggravating the milieu of male fertility and spermatogenesis. H 2 regulates intracellular MAPK downstream cAMP signal and Ca 2+ signal as a signal modulator to antagonize ROS signaling. Thus H 2 can play a role in modulating signals involved in testosterone hormone production to improve male fertility caused by redox imbalance. We therefore hypothesize that molecular hydrogen may enhance testosterone production via cellular redox balance. By this hypothesis, we anticipate that molecular hydrogen may be an effective remedy in male infertility.

Original languageEnglish
Pages (from-to)6-9
Number of pages4
JournalMedical Hypotheses
Publication statusPublished - 2018 Dec

Bibliographical note

Funding Information:
This work was supported by the Ministry of Education of the Republic of Korea and the National Research Foundation of Korea ( NRF-2016S1A5B8925203 ).

Publisher Copyright:
© 2018 Elsevier Ltd

All Science Journal Classification (ASJC) codes

  • Medicine(all)


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