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Background  Iron plays a pivotal role in the pathogenesis of  Trichomonas vaginalis , the causative agent of highly prevalent human trichomoniasis.  T. vaginalis  resides in the vaginal region, where the iron concentration is constantly changing. Hence,  T. vaginalis  must adapt to variations in iron availability to establish and maintain an infection. The free radical signaling molecules reactive oxygen species (ROS) and reactive nitrogen species (RNS) have been proven to participate in iron deficiency in eukaryotes. However, little is known about the roles of these molecules in iron-deficient  T. vaginalis .    Methods   T. vaginalis  cultured in iron-rich and -deficient conditions were collected for all experiments in this study. Next generation RNA sequencing was conducted to investigate the impact of iron on transcriptome of  T. vaginalis . The cell viabilities were monitored after the trophozoites treated with the inhibitors of nitric oxide (NO) synthase (L-NG-monomethyl arginine, L-NMMA) and proteasome (MG132). Hydrogenosomal membrane potential was measured using JC-1 staining.    Results  We demonstrated that NO rather than ROS accumulates in iron-deficient  T. vaginalis.  The level of NO was blocked by MG132 and L-NMMA, indicating that NO production is through a proteasome and arginine dependent pathway. We found that the inhibition of proteasome activity shortened the survival of iron-deficient cells compared with untreated iron-deficient cells. Surprisingly, the addition of arginine restored both NO level and the survival of proteasome-inhibited cells, suggesting that proteasome-derived NO is crucial for cell survival under iron-limited conditions. Additionally, NO maintains the hydrogenosomal membrane potential, a determinant for cell survival, emphasizing the cytoprotective effect of NO on iron-deficient  T. vaginalis . Collectively, we determined that NO produced by the proteasome prolonged the survival of iron-deficient  T. vaginalis  via maintenance of the hydrogenosomal functions.    Conclusion  The findings in this study provide a novel role of NO in adaptation to iron-deficient stress in  T. vaginalis  and shed light on a potential therapeutic strategy for trichomoniasis.    Electronic supplementary material  The online version of this article (doi:10.1186/s13071-015-1000-5) contains supplementary material, which is available to authorized users.

Nitric oxide maintains cell survival of Trichomonas vaginalis upon iron depletion