Search for: All records

ABSTRACT Gill regeneration in fish varies inter- and intra-specifically. The latter may be associated with myriad factors including capacity of energy metabolism. This study investigated whether mitochondrial respiration capacity influences the degree of gill regeneration and features of mitochondria in regenerated tissue by feeding fish an experimental diet aimed at modulating mitochondrial efficiency. Atlantic salmon reared on standard and experimental diet were subjected to 50% filament resection on a subset of filaments on the ventral and dorsal regions of the first gill arch. Mitochondrial respiration and citrate synthase activity (CSA) were measured in the resected tips of filaments (week-0) and then in the regenerated tissue at 20 weeks post-resection (week-20). The degree of filament regeneration was measured at week-20. The experimental diet reduced CSA and respiratory control ratio (RCR), and increased proton leak at week-0, which was associated with a 30% reduction in tissue regeneration compared with fish on standard diet. While CSA increased in the regenerated tissue of experimental diet fish, there was a decline in other metrics of mitochondrial respiration including state 3, proton leak and RCR irrespective of diet. Overall, mitochondrial respiration efficiency at week-0 was positively correlated with the degree of subsequent gill tissue regeneration. Additionally, state 3 respiration and proton leak at week-20 were positively correlated with tissue regeneration, whereas CSA exhibited a negative relationship. Our results indicate that the capacity of mitochondrial respiration may at least partially explain the inter-individual variation in tissue regeneration, but mitochondrial function in the regenerating tissue may be limited. 

The acid–base relevant molecules carbon dioxide (CO2), protons (H+), and bicarbonate (HCO3−) are substrates and end products of some of the most essential physiological functions including aerobic and anaerobic respiration, ATP hydrolysis, photosynthesis, and calcification. The structure and function of many enzymes and other macromolecules are highly sensitive to changes in pH, and thus maintaining acid–base homeostasis in the face of metabolic and environmental disturbances is essential for proper cellular function. On the other hand, CO2, H+, and HCO3− have regulatory effects on various proteins and processes, both directly through allosteric modulation and indirectly through signal transduction pathways. Life in aquatic environments presents organisms with distinct acid–base challenges that are not found in terrestrial environments. These include a relatively high CO2 relative to O2 solubility that prevents internal CO2/HCO3 − accumulation to buffer pH, a lower O2 content that may favor anaerobic metabolism, and variable environmental CO2, pH and O2 levels that require dynamic adjustments in acid–base homeostatic mechanisms. Additionally, some aquatic animals purposely create acidic or alkaline microenvironments that drive specialized physiological functions. For example, acidifying mechanisms can enhance O2 delivery by red blood cells, lead to ammonia trapping for excretion or buoyancy purposes, or lead to CO2 accumulation to promote photosynthesis by endosymbiotic algae. On the other hand, alkalinizing mechanisms can serve to promote calcium carbonate skeletal formation. This nonexhaustive review summarizes some of the distinct acid–base homeostatic mechanisms that have evolved in aquatic organisms to meet the particular challenges of this environment. 

Previously, we showed that the evolution of high acuity vision in fishes was directly associated with their unique pH-sensitive hemoglobins that allow O 2 to be delivered to the retina at PO 2 s more than ten-fold that of arterial blood (Damsgaard et al., 2019). Here, we show strong evidence that vacuolar-type H + -ATPase and plasma-accessible carbonic anhydrase in the vascular structure supplying the retina act together to acidify the red blood cell leading to O 2 secretion. In vivo data indicate that this pathway primarily affects the oxygenation of the inner retina involved in signal processing and transduction, and that the evolution of this pathway was tightly associated with the morphological expansion of the inner retina. We conclude that this mechanism for retinal oxygenation played a vital role in the adaptive evolution of vision in teleost fishes.