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The volcano rabbit ( Romerolagus diazi ) is a lagomorph endemic to the central mountains of the Trans-Mexican Volcanic Belt and is classified as threatened at extinction risk. It is a habitat specialist in bunchgrass communities. The annual wildfires that occur throughout its distribution range are a vulnerability factor for the species. However, the effects of wildfires on volcano rabbit populations are not fully understood. We evaluated the occupancy and change in the volcano rabbit relative abundance index in the burned bunchgrass communities of the Ajusco-Chichinautzin Mountain Range during an annual cycle of wildfire events. Additionally, we assessed the factors that favor and limit occupation and reoccupation by the volcano rabbit using the relative abundance index in burned plots as an indicator of these processes. The explanatory factors for the response of the volcano rabbit were its presence in the nearby unburned bunchgrasses, the height of three species of bunchgrass communities, the proportion of different types of vegetation cover within a 500 m radius around the burned plots, heterogeneity of the vegetation cover, and the extent of the wildfire. Statistical analyses indicated possible reoccupation in less than a year in burned bunchgrass communities adjacent to unburned bunchgrass communities with volcano rabbits. The relative abundance index of volcano rabbits was not favored when the maximum height of the Muhlenbergia macroura bunchgrass community was less than 0.77 m. When the vegetation around the burned plots was dominated by forest (cover >30% of the buffer) and the fire was extensive, the number of latrines decreased per month but increased when the bunchgrass and shrub cover was greater around the burned plots. While the statistical results are not conclusive, our findings indicate a direction for future projects, considering extensive monitoring to obtain a greater number of samples that contribute to consolidating the models presented., Competing Interests: This research is part of the Doctoral dissertation of Juan Manuel Uriostegui Velarde (CONACyT scholarship 281981) presented at the Instituto de Ecología, A. C., (© 2024 Uriostegui-Velarde et al.)

Peroxiredoxin 6 (Prdx6) repairs peroxidized membranes by reducing oxidized phospholipids, and by replacing oxidized sn-2 fatty acyl groups through hydrolysis/reacylation by its phospholipase A 2 (aiPLA 2 ) and lysophosphatidylcholine acyltransferase activities. Prdx6 is highly expressed in the lung, and intact lungs and cells null for Prdx6 or with single-point mutations that inactivate either Prdx6-peroxidase or aiPLA 2 activity alone exhibit decreased viability, increased lipid peroxidation, and incomplete repair when exposed to paraquat, hyperoxia, or organic peroxides. Ferroptosis is form of cell death driven by the accumulation of phospholipid hydroperoxides. We studied the role of Prdx6 as a ferroptosis suppressor in the lung. We first compared the expression Prdx6 and glutathione peroxidase 4 (GPx4) and visualized Prdx6 and GPx4 within the lung. Lung Prdx6 mRNA levels were five times higher than GPx4 levels. Both Prdx6 and GPx4 localized to epithelial and endothelial cells. Prdx6 knockout or knockdown sensitized lung endothelial cells to erastin-induced ferroptosis. Cells with genetic inactivation of either aiPLA 2 or Prdx6-peroxidase were more sensitive to ferroptosis than WT cells, but less sensitive than KO cells. We then conducted RNA-seq analyses in Prdx6-depleted cells to further explore how the loss of Prdx6 sensitizes lung endothelial cells to ferroptosis. Prdx6 KD upregulated transcriptional signatures associated with selenoamino acid metabolism and mitochondrial function. Accordingly, Prdx6 deficiency blunted mitochondrial function and increased GPx4 abundance whereas GPx4 KD had the opposite effect on Prdx6. Moreover, we detected Prdx6 and GPx4 interactions in intact cells, suggesting that both enzymes cooperate to suppress lipid peroxidation. Notably, Prdx6-depleted cells remained sensitive to erastin-induced ferroptosis despite the compensatory increase in GPx4. These results show that Prdx6 suppresses ferroptosis in lung endothelial cells and that both aiPLA 2 and Prdx6-peroxidase contribute to this effect. These results also show that Prdx6 supports mitochondrial function and modulates several coordinated cytoprotective pathways in the pulmonary endothelium., Competing Interests: Declaration of competing interest The authors declare the following financial interests/personal relationships which may be considered as potential competing interests: Jose Pablo Vazquez-Medina reports financial support was provided by National Institute of General Medical Sciences. Jose Pablo Vazquez-Medina reports a relationship with National Institute of General Medical Sciences that includes: funding grants. If there are other authors, they declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Background: Elephant seals exhibit extreme hypoxemic tolerance derived from repetitive hypoxia/reoxygenation episodes they experience during diving bouts. Real-time assessment of the molecular changes underlying protection against hypoxic injury in seals remains restricted by their at-sea inaccessibility. Hence, we developed a proliferative arterial endothelial cell culture model from elephant seals and used RNA-seq, functional assays, and confocal microscopy to assess the molecular response to prolonged hypoxia., Results: Seal and human endothelial cells exposed to 1% O 2 for up to 6 h respond differently to acute and prolonged hypoxia. Seal cells decouple stabilization of the hypoxia-sensitive transcriptional regulator HIF-1α from angiogenic signaling. Rapid upregulation of genes involved in glutathione (GSH) metabolism supports the maintenance of GSH pools, and intracellular succinate increases in seal but not human cells. High maximal and spare respiratory capacity in seal cells after hypoxia exposure occurs in concert with increasing mitochondrial branch length and independent from major changes in extracellular acidification rate, suggesting that seal cells recover oxidative metabolism without significant glycolytic dependency after hypoxia exposure., Conclusions: We found that the glutathione antioxidant system is upregulated in seal endothelial cells during hypoxia, while this system remains static in comparable human cells. Furthermore, we found that in contrast to human cells, hypoxia exposure rapidly activates HIF-1 in seal cells, but this response is decoupled from the canonical angiogenesis pathway. These results highlight the unique mechanisms that confer extraordinary tolerance to limited oxygen availability in a champion diving mammal., (© 2024. The Author(s).)