Background: We aimed to investigate the correlation between hepcidin mRNA expression and the pathophysiology of the liver or the long-term prognosis in patients with chronic hepatitis C (CHC) or liver cirrhosis (LC).

Methods: A total of 82 patients with CHC or LC who underwent liver biopsy were included in this study. Hepcidin mRNA expression was detected in the frozen liver tissues obtained from patients with CHC or LC who underwent liver biopsy. Hepcidin mRNA expression in frozen liver tissues was assessed using real-time quantitative polymerase chain reaction. We previously reported that the extent of proliferation of atypical hepatocytes (POAH) within the six-cell lesion of irregular regeneration (IR) of hepatocytes is a significant histological finding associated with the development of hepatocellular carcinoma (HCC) from CHC or LC. Therefore, we investigated the association between hepcidin mRNA expression and disease severity, pathological findings such as the extent of POAH, and the incidence of HCC development from CHC and LC. Furthermore, we compared hepcidin mRNA expression with serum cytokine and chemokine levels using a Bio-plex suspension array system (Bio-Rad Laboratories, CA, USA).

Results: Hepcidin mRNA expression was associated with serum ferritin concentration (p=0.009) and unsaturated iron-binding capacity (P=0.0003) in the serological parameters, but no association was found with histological parameters. The cumulative incidence of HCC development was significantly higher in the low hepcidin mRNA expression group than in the high hepcidin mRNA expression group (p=0.003). Additionally, patients with lower hepcidin mRNA levels tended to exhibit more extensive POAH (p=0.0089). Hepcidin mRNA expression was also significantly associated with apoptosis-related and anti-inflammatory cytokines/chemokines.

Conclusions: Low hepcidin mRNA expression may be a risk factor for carcinogenesis in patients with CHC or LC.

Escherichia coli uses selenite as a nutritional selenium source for the synthesis of selenoproteins, and excess selenite is converted to elemental selenium nanoparticles (SeNPs) through a detoxification process. The reduction of selenite is thought to be facilitated by two major redox systems: the thioredoxin (Trx) system and glutathione (GSH) system. However, the extent to which these redox systems are involved in selenoprotein synthesis and SeNP formation remains unclear. In this study, we investigated the effects of gene disruption in the Trx (trxA, trxB, and trxC) and GSH (gshB and gor) systems on SeNP formation, selenite sensitivity, and selenoprotein synthesis in E. coli. We found that the disruption of a single gene in either the Trx or GSH system did not drastically affect SeNP formation via selenite reduction in the presence of 1 mM selenite. However, trxB, gshB, and gor were observed to be important for the tolerance of the bacterium to > 5 mM selenite. The ΔtrxA and ΔtrxB strains exhibited lower activity of the selenoprotein formate dehydrogenase as compared to the wild-type strain, suggesting that trxA and trxB are important for selenoprotein biosynthesis. Selenite detoxification via SeNP formation involves both the Trx and GSH systems, but selenoprotein biosynthesis specifically depends on the Trx system.