Sodium Sulfite as a Novel Hypoxia Revulsant Involved in Hypoxic Regulation in Escherichia coli.

As a reducing salt, sodium sulfite could deprive oxygen in solution, which could mimic hypoxic stress in Caenorhabditis elegans. In this study, the wild-type Escherichia coli strain MG1655 was used to examine the inhibition of sodium sulfite-induced hypoxia by observing the bacterial growth curves. We also analyzed the growth curves of mutant strains (for arcA/B, soxR/S, fnr, and oxyR) related to E. coli hypoxic pathways to reveal roles of the related genes during hypoxia. The ultrastructure of hypoxia-inhibited bacteria were also observed using transmission electron microscopy. Sodium sulfite could maintain hypoxic condition of bacterial culture for 8 h with concentrations over 40 mmol/L. Complete ultrastructure of the bacteria indicated sodium sulfite did inhibit bacterial growth and division. Among the hypoxia genes, fnr and arcB played key roles in sodium sulfite-induced hypoxia. This study showed that sodium sulfite could be used as a novel hypoxia revulsant for bacterial cultures.

Loss of nuclear ARC contributes to the development of cardiac hypertrophy in rats.

AIM: Cardiac hypertrophy and myocardial apoptosis are two major factors in heart failure. As a classical regulator of apoptosis, apoptosis repressor with caspase recruitment domain (ARC) has recently also been found to have a protective effect against hypertrophy. However, the mechanism underlying this effect is still not fully understood. METHODS: In the present study, we established animal and cellular models to monitor the changes in total and nuclear ARC during cardiac hypertrophic processes. The preventive effects of nuclear ARC in cellular hypertrophy were verified by ARC regulation and nuclear export inhibition. To further explore the mechanism for nuclear ARC superficially, we analysed proteins that interact with ARC in the nucleus via Co-IP and mass spectrometry. RESULTS: The expression of total ARC in hypertrophic myocardial tissue and H9C2 cells remained invariant, while the level of nuclear ARC decreased dramatically. By altering the content of ARC in H9C2 cells, we found that both nuclear ARC transfection and nuclear ARC export blockade attenuated norepinephrine or angiotensin II-induced hypertrophy, while ARC knockdown had an inverse effect. Co-IP data showed that ARC interacted with prohibitin (PHB) in the nucleus and might participate in maintaining the level of PHB in cells. CONCLUSIONS: These findings suggest a novel mechanism for ARC in cardiac hypertrophy prevention and also indicate that the anti-hypertrophic roles of ARC are probably associated with its localization in nucleus, which imply the nuclear ARC as a potential therapeutic target for cardiac hypertrophy.