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Bacterial translocation into portal blood from the gut could be detected as early as 15 min following portal triad occlusion (PTO) in rats and increased with the increasing length of PTO. The peak of bacterial translocation was between 60 and 90 min in the experimental model of PTO for 120 min. The mean counts per minute (cpm) of radiolabelled Escherichia coli in groups with PTO for 60 and 90 min were 5 and 6 times higher in portal blood and 3 and 4 times higher in the systemic circulation than control rats (p < 0.05). Plasma endotoxin levels in portal and systemic blood were significantly increased. The laser blood flow of the intestinal loops and the ileocecal mucosal surface and the mean portal pO₂ were profoundly declined in all experimental groups during PTO. We found that the elevation in cpm of radiolabelled bacteria is directly proportional to the increased endotoxin levels in portal and systemic blood and is inversely proportional to the decreased flux values of blood flow in the intestinal loop and the ileocecal mucosal surface. These findings indicate that there may be an intimate relationship between bacterial translocation into portal blood from the gut, acute gut barrier dysfunction resulting from the decrease in blood flow of the gastrointestinal tract, the increases in the endotoxin level in portal blood, and the reduction in portal pO₂ during PTO.

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The mortality rate of idiopathic pulmonary fibrosis (IPF) increases yearly due to ineffective treatment. Given that the lung is exposed to the external environment, it is likely that oxidative stress, especially the stimulation of DNA, would be of particular importance in pulmonary fibrosis. DNA damage is known to play an important role in idiopathic pulmonary fibrosis initiation, so DNA repair systems targeting damage are also crucial for the survival of lung cells. Although many contemporary reports have summarized the role of individual DNA damage and repair pathways in their hypotheses, they have not focused on idiopathic pulmonary fibrosis. This review, therefore, aims to provide a concise overview for researchers to understand the pathways of DNA damage and repair and their roles in IPF.