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Biology subjects

Melancon, V.

Publications and source records attributed to Melancon, V..

4 recordsLinked to original sources

Alterations to cellular metabolism are linked to multiple natural parasite infections across populations of a freshwater fish

Exposure to environmental stressors can induce physiological responses in organisms, which can lead to population-level differences in physiological traits. However, the mechanisms underlying these responses both within individuals and among populations are often unknown. Parasite infections, in particular, are important biotic stressors that can induce a range of effects in hosts, including altered whole-organism metabolism. However, few studies have explored sub-cellular alterations to metabolic performance across both an individual infection gradient and population-level differences in infection prevalence. We compared mitochondrial enzyme activities across five distinct populations of pumpkinseed sunfish (Lepomis gibbosus) differing in the prevalence of cestode and trematode parasites. Overall, we found that enzymes from the OXPHOS pathway (cytochrome c oxidase, NADH dehydrogenase and coenzyme Q : cytochrome c oxidoreductase), the anaerobic pathway (lactate dehydrogenase), the TCA cycle (citrate synthase) and lipid metabolism (carnitine palmitoyl transferase) were positively correlated with parasite density with trends depending on the organ, parasite species and host population studied. Our results suggest complex and nuanced relationships among infections and host physiological performance and provide strong evidence of parasite-induced alterations to mitochondrial metabolism which may explain previously reported whole-organism responses to infections.

ecology↗

Evaluation of parasitic contamination and effects on estimates of mitochondrial enzymatic activities in infected fish livers

Parasites can impair host performance through various physiological processes, including alterations to host metabolism. Since mitochondria are responsible for cellular energy production, it is likely that disruptions in host cellular metabolism contribute to changes in metabolism at the organismal level. However, some studies investigating parasite-induced alteration in cellular metabolism have not taken the presence of parasites in the target tissues into account, potentially biasing results. It is therefore critical to confirm that the measured enzyme activities reflect those of the hosts rather than the parasites themselves. Here, we tested a parasite extraction protocol to evaluate the extent to which parasite contamination impacts estimates of cellular enzyme activities in hepatic tissues of wild pumpkinseed sunfish (Lepomis gibbosus) infected with bass tapeworm cestodes (Proteocephalus ambloplitis). We tested four treatments: uninfected livers, cleaned infected livers, infected livers (repopulated) and parasites alone. We then compared the activity of key metabolic enzymes among groups. PCR tests were used to assess parasitic contamination of samples after applying the parasite extraction protocol on hepatic tissue. Enzyme activities of cleaned livers and contaminated livers were similar despite PCR tests revealing contamination. The intensity of cestode infection also did not influence enzyme activity, which suggests that parasite presence in liver tissues does not impact the accuracy of the enzyme activity estimates. These results suggest that studying the organs of heavily parasitized individuals is possible. Nevertheless, we recommend that our cleaning protocol is applied to infected organs to avoid any perception of biases in highly infected individuals.

ecology↗

Acclimation temperature and parasite infection drive metabolic changes in a freshwater fish at different biological scales

O_LIEnvironmental stressors such as elevated temperature and parasite infection can impact individual energy metabolism. However, organismal responses to co-occurring stressors and their effects across biological scales remain unexplored despite the importance of integrative studies for accurately predicting the resilience of natural populations in changing environments. C_LIO_LIUsing wild-caught, naturally parasitized pumpkinseed sunfish, Lepomis gibbosus, we quantified changes in cellular and whole-organism metabolism in response to temperature and parasite infection. We acclimated pumpkinseeds for three weeks at 20{degrees}C, 25{degrees}C, or 30{degrees}C before measuring whole-organism oxygen uptake ([M]O2) using intermittent flow-respirometry to quantify maximal and standard metabolic rates (MMR and SMR, respectively) and aerobic scope (AS). We also measured the maximal activity of enzymes (citrate synthase (CS), respiratory complexes I + III and IV of the electron transport system, and lactate dehydrogenase (LDH)) linked with cellular bioenergetics in fish heart, brain, spleen and gills using spectrophotometry. C_LIO_LIWe found no interactions between acclimation temperatures and parasite intensity on cellular or whole-organism metabolism. However, both stressors were independently related to fish metabolism, with differing impacts across biological scales. C_LIO_LIWhereas MMR increased with acclimation temperature, this was not mirrored by increasing SMR or decreasing AS, suggesting thermal compensation across acclimation temperatures at the whole-organism level. C_LIO_LIOn a cellular level, acclimation responses were similar across organs, with maximal activity of all enzymes decreasing with increasing acclimation temperature. However, LDH activity remained higher than aerobic enzyme activities (CS, ETS complexes I + III and IV) across acclimation temperatures and organs, especially in gills, where LDH activity drastically increased at 30{degrees}C. This may indicate a stronger reliance on anaerobic metabolism to sustain whole-organism metabolic performance. C_LIO_LIFish with greater trematode infection had lower MMR and AS. There were no relationships between parasite intensity and SMR nor maximal enzyme activity. C_LIO_LIOur work shows that co-occurring stressors have distinct impacts on fish metabolism: parasites are primarily related to whole-organism metabolism while temperature impacts metabolism across biological scales. This highlights that interactions among co-occurring stressors are important for ecological realism and accurate predictions regarding population resilience to environmental changes. C_LI

physiology↗

Mitochondrial metabolism and body condition of naturally infected sunfish (Lepomis gibbosus)

Parasites can affect host behavior, cognition, locomotion, body condition and many other physiological traits. Changes to host aerobic metabolism are likely responsible for these parasite-induced performance alterations. Whole-organism metabolic rate is underpinned by cellular energy metabolism driven most prominently by the mitochondria. However, few studies have explored how mitochondrial enzymatic activity relates to body condition and parasite infection despite being a putative site for metabolic disruptions related to health status. We studied correlations among natural parasite infection, host body condition and the activity of key mitochondrial enzymes in target organs from wild-caught pumpkinseed sunfish (Lepomis gibbosus) to better understand the cellular responses of fish hosts to endoparasite infection. Enzymatic activities in the gills, spleen, and brain of infected fish were not significantly related to parasite infection or host body condition. However, the activity of cytochrome C oxidase, an enzyme involved in oxidative phosphorylation, in fish hearts was higher in individuals with lower body condition. Activities of citrate synthase, complexes I and III and carnitine palmitoyltransferase were also significantly different among organ types. These results provide preliminary information regarding the likely mitochondrial pathways affecting host body condition, the maintenance energetic requirements of different organs and their specific dependency on particular mitochondrial pathways. These results help pave the way for future studies on the effects of parasite infection on mitochondrial metabolism.

ecology↗