Biology subjects

Pichaud, N.

Publications and source records attributed to Pichaud, N..

3 recordsLinked to original sources

bioRxiv2025

Multigenerational effects of temperature exposure on upper thermal limit and mitochondrial functioning in Medaka (Oryzias Latipes) brain

Determining the mechanisms underpinning the thermal limits of organisms is essential to anticipate the impact of climate change on their survival. As mitochondrial activity is key for cellular ATP production, we aimed at investigating the link between mitochondrial dysfunction and the upper thermal limit (CTmax) at which neuromuscular functions are lost. We reared medaka fish (Oryzias latipes) over generations at 20{degrees}C (COLD) and 30{degrees}C (WARM) during five years and measured their CTmax and their mitochondrial oxygen consumption rates (OCRs) at 25{degrees}C and at their CTmax. We found that multigenerational exposure at elevated temperature increases the CTmax by 13%. We observed for all fish a general decrease in the OCRs and for the RCR of complex-I between 25{degrees}C and their CTmax suggesting a link between CTmax and cerebral mitochondrial performance. Finally, we found an increase in the contribution of the mitochondria complex II to OCRs at elevated temperature suggesting that this complex underlie the plasticity in mitochondrial functioning at high temperature. Our study highlights the link between whole organism thermal tolerance and mitochondrial dysfunction and that multigenerational exposure can modify mitochondrial and thermal performance.

ecology↗

bioRxiv2022

Phenotypic plasticity during diel cycling hypoxia in Arctic char (Salvelinus alpinus)

Oxygen concentration naturally fluctuates in aquatic environments. Due to increased eutrophication caused by anthropic activities, this phenomenon could be amplified and result in a daily cycle of alternating normoxic and hypoxic conditions. At the metabolic level, lack of oxygen and reoxygenation can both have serious repercussions on fish due to fluctuations in ATP supply and demand and an elevated risk of oxidative burst. Thus, fish must adjust their phenotype to survive and equilibrate their energetic budget. However, their energy allocation strategy could imply a reduction in growth which could be deleterious for their fitness. Although the impact of cyclic hypoxia is a major issue for ecosystems and fisheries worldwide, our knowledge remains however limited. Our objective was to characterise the effects of cyclic hypoxia on growth and metabolism in fish. We monitored growth parameters (specific growth rate, condition factor), hepatosomatic and visceral indexes, relative heart mass and hematocrit of Arctic char (Salvelinus alpinus) exposed to thirty days of cyclic hypoxia. We also measured the hepatic protein synthesis rate, hepatic triglycerides as well as muscle glucose, glycogen and lactate, and quantified hepatic metabolites during this treatment. Arctic char appeared to acclimate well to oxygen fluctuations. The first days of cyclic hypoxia induced a profound metabolome reorganisation in the liver. However, fish rebalanced their metabolic activities and successfully maintained their growth and energetic reserves after one month of cyclic hypoxia. These results demonstrate the impressive ability of fish to cope with their changing environment. Summary statementThis study characterizes the metabolic adjustments performed by Arctic char when coping with one month of cyclic hypoxia. Fish reached a new phenotype by defending their growth and energy stores.

physiology↗

bioRxiv2020

Dramatic changes in mitochondrial substrate use at critically high temperatures: a comparative study using Drosophila

Ectotherm thermal tolerance is critical to species distribution, but at present the physiological underpinnings of heat tolerance remain poorly understood. Mitochondrial function is perturbed at critically high temperatures in some ectotherms, including insects, suggesting that heat tolerance of these animals is linked to failure of oxidative phosphorylation (OXPHOS) and/or ATP production. To test this hypothesis we measured mitochondrial oxygen consumption rates in six Drosophila species with different heat tolerance using high-resolution respirometry. Using a substrate-uncoupler-inhibitor titration protocol we examined specific steps of the electron transport system to study how temperatures below, bracketing and above organismal heat limits affected mitochondrial function and substrate oxidation. At benign temperatures (19 and 30{degrees}C), complex I-supported respiration (CI-OXPHOS) was the most significant contributor to maximal OXPHOS. At higher temperatures (34, 38, 42 and 46{degrees}C), CI-OXPHOS decreased considerably, ultimately to very low levels at 42 and 46{degrees}C. The enzymatic catalytic capacity of complex I was intact across all temperatures and accordingly the decreased CI-OXPHOS is unlikely to be caused directly by hyperthermic denaturation/inactivation of complex I. Despite the reduction in CI-OXPHOS, maximal OXPHOS capacities were maintained in all species, through oxidation of alternative substrates; proline, succinate and, particularly, glycerol-3-phosphate, suggesting important mitochondrial flexibility at temperatures exceeding the organismal heat limit. Interestingly, this compensatory oxidation of alternative substrates occurred at temperatures that tended to correlate with species heat tolerance, such that heat-tolerant species could defend "normal" mitochondrial function at higher temperatures than sensitive species. Future studies should investigate why CI-OXPHOS is perturbed and how this potentially affects ATP production rates.

physiology↗