Changes in liver and lung antioxidant and mitochondrial biogenesis gene expression in decompression sickness...

Susceptibility to decompression sickness (DCS) shows wide interindividual variability, the origins of which remain poorly understood. To better elucidate its mechanisms, we previously developed a rat strain with more than threefold higher resistance to DCS through selective breeding. In this study, we examined baseline expression of genes related to antioxidant defense and mitochondrial biogenesis in the lungs and liver of DCS-resistant and nonresistant Wistar rats. None of the animals were exposed to hyperbaric conditions, allowing us to focus on constitutive expression differences potentially underlying genetic resistance to DCS. Quantitative reverse transcription polymerase chain reaction was performed, and data were analyzed using two-way ANOVA to assess the effects of selection, sex, and their interaction. In the lungs, no significant selection effect was observed for genes involved in mitochondrial biogenesis (Pgc1α, Nrf1, and Nrf2) or antioxidant defense (Sod1, Sod2, Gpx1, and Cat). In contrast, in the liver, expression of both gene groups was significantly decreased in resistant rats (P < 0.0083, Bonferroni correction), except for Pgc1α. These lower hepatic expression levels align with the previously reported reduction in citrate synthase activity and lower basal oxygen consumption in the soleus muscle of resistant rats. Together, these findings suggest that hepatic metabolism and mitochondrial function may play key roles in DCS susceptibility, potentially through reduced mitochondrial activity and lower reactive oxygen species production in resistant animals.NEW & NOTEWORTHY This study analyzed genes related to antioxidant defense and mitochondrial biogenesis in the lungs and liver of rats bred for resistance to decompression sickness (DCS). In resistant rats, no change was observed in lung gene expression, whereas both gene groups were downregulated in the liver (P < 0.0083, Bonferroni correction), except Pgc1α. These findings, along with previous ones, suggest that hepatic mitochondrial function and reduced reactive oxygen species production may contribute to DCS resistance.