Cookies help us deliver our services. By using our services, you agree to our use of cookies. More information

Difference between revisions of "Saleem 2023 MiPschool Obergurgl"

From Bioblast
(Created page with "{{Abstract |title=left|100px|Mitochondrial Physiology Society|MiPsociety Mitochondrial physiology in cardiac muscle of deer mice native to high al...")
 
Line 1: Line 1:
{{MiP header page name}}
{{Abstract
{{Abstract
|title=[[Image:MiPsocietyLOGO.JPG|left|100px|Mitochondrial Physiology Society|MiPsociety]] Mitochondrial physiology in cardiac muscle of deer mice native to high altitude.
|title=[[Image:MiPsocietyLOGO.JPG|left|100px|Mitochondrial Physiology Society|MiPsociety]] Mitochondrial physiology in cardiac muscle of deer mice native to high altitude.
Line 5: Line 6:
|year=2023
|year=2023
|event=MiPschool Obergurgl 2023
|event=MiPschool Obergurgl 2023
|abstract=Authors: Saleem Ranim,   Scott GR<br>
|abstract='''Authors:''' [[Saleem Ranim]], [[Scott Graham R]]<br>


Introduction: High-altitude environments are characterized by cold temperatures and low O2 levels (hypoxia). Small mammals at high altitude thus face the metabolic challenge of maintaining thermogenesis to cope with cold in a hypoxic environment that can constrain aerobic ATP supply. Circulatory O2 delivery by the heart is essential for supporting tissue O2 demands, but it is unclear whether evolved or plastic changes in cardiac mitochondria help overcome constraints on thermogenesis in high-altitude environments.
'''Introduction:''' High-altitude environments are characterized by cold temperatures and low O<sub>2</sub> levels (hypoxia). Small mammals at high altitude thus face the metabolic challenge of maintaining thermogenesis to cope with cold in a hypoxic environment that can constrain aerobic ATP supply. Circulatory O<sub>2</sub> delivery by the heart is essential for supporting tissue O<sub>2</sub> demands, but it is unclear whether evolved or plastic changes in cardiac mitochondria help overcome constraints on thermogenesis in high-altitude environments.<br>
Method: We examined this issue in deer mice (Peromyscus maniculatus). Mice from populations native to high altitude and low altitude were born and raised in captivity, and adults were acclimated to warm (25C) normoxia or cold (5C) hypoxia (~12 kPa O2 for 5-6 weeks) in a full-factorial design. Mitochondrial function was studied by high-resolution respirometry and fluorometry in permeabilized tissue from left ventricles and was complemented by assays of several metabolic and antioxidant enzymes.
'''Method:''' We examined this issue in deer mice (Peromyscus maniculatus). Mice from populations native to high altitude and low altitude were born and raised in captivity, and adults were acclimated to warm (25 °C) normoxia or cold (5 °C) hypoxia (~12 kPa O<sub>2</sub> for 5-6 weeks) in a full-factorial design. Mitochondrial function was studied by high-resolution respirometry and fluorometry in permeabilized tissue from left ventricles and was complemented by assays of several metabolic and antioxidant enzymes.<br>
Results and discussion: Mitochondrial capacities for oxidative phosphorylation and electron transport were similar between populations and were unaffected by acclimation to cold hypoxia, as were activities of citrate synthase and cytochrome oxidase. However, exposure to cold hypoxia increased activities of lactate dehydrogenase, which were also greater in highlanders than in lowlanders, likely to augment capacities for lactate oxidation. Furthermore, mitochondrial emission of reactive oxygen species was lower in highlanders than in lowlanders across environments, associated with lower levels of lipid peroxidation and protein carbonyls. Therefore, phenotypic plasticity and evolved changes in cardiac mitochondria help deer mice cope with metabolic challenges at high altitude
'''Results and discussion:''' Mitochondrial capacities for oxidative phosphorylation and electron transport were similar between populations and were unaffected by acclimation to cold hypoxia, as were activities of citrate synthase and cytochrome oxidase. However, exposure to cold hypoxia increased activities of lactate dehydrogenase, which were also greater in highlanders than in lowlanders, likely to augment capacities for lactate oxidation. Furthermore, mitochondrial emission of reactive oxygen species was lower in highlanders than in lowlanders across environments, associated with lower levels of lipid peroxidation and protein carbonyls. Therefore, phenotypic plasticity and evolved changes in cardiac mitochondria help deer mice cope with metabolic challenges at high altitude.<br>
|keywords=High-altitude hypoxia, deer mice, cardiac mitochondria, reactive oxygen species
|keywords=High-altitude hypoxia, deer mice, cardiac mitochondria, reactive oxygen species
|mipnetlab=CA Hamilton Scott GR
|mipnetlab=CA Hamilton Scott GR
}}
}}
== Affiliation ==
::::Saleem Ranim,  Scott GR
:::::Department of Biology, McMaster University, Hamilton, Ontario, Canada
:::: Corresponding author: saleer4@mcmaster.ca
{{Labeling
{{Labeling
|injuries=Temperature, Hypoxia
|injuries=Temperature, Hypoxia

Revision as of 18:26, 30 March 2023

MiPsociety
       
MitoGlobal
       
MitoGlobal Events
       
MiPconference
       
MiPschool 2023
       


Saleem 2023 MiPschool Obergurgl

MiPsociety
Mitochondrial physiology in cardiac muscle of deer mice native to high altitude.

Link: MiPschool Obergurgl 2023

Saleem Ranim (2023)

Event: MiPschool Obergurgl 2023

Authors: Saleem Ranim, Scott Graham R

Introduction: High-altitude environments are characterized by cold temperatures and low O2 levels (hypoxia). Small mammals at high altitude thus face the metabolic challenge of maintaining thermogenesis to cope with cold in a hypoxic environment that can constrain aerobic ATP supply. Circulatory O2 delivery by the heart is essential for supporting tissue O2 demands, but it is unclear whether evolved or plastic changes in cardiac mitochondria help overcome constraints on thermogenesis in high-altitude environments.
Method: We examined this issue in deer mice (Peromyscus maniculatus). Mice from populations native to high altitude and low altitude were born and raised in captivity, and adults were acclimated to warm (25 °C) normoxia or cold (5 °C) hypoxia (~12 kPa O2 for 5-6 weeks) in a full-factorial design. Mitochondrial function was studied by high-resolution respirometry and fluorometry in permeabilized tissue from left ventricles and was complemented by assays of several metabolic and antioxidant enzymes.
Results and discussion: Mitochondrial capacities for oxidative phosphorylation and electron transport were similar between populations and were unaffected by acclimation to cold hypoxia, as were activities of citrate synthase and cytochrome oxidase. However, exposure to cold hypoxia increased activities of lactate dehydrogenase, which were also greater in highlanders than in lowlanders, likely to augment capacities for lactate oxidation. Furthermore, mitochondrial emission of reactive oxygen species was lower in highlanders than in lowlanders across environments, associated with lower levels of lipid peroxidation and protein carbonyls. Therefore, phenotypic plasticity and evolved changes in cardiac mitochondria help deer mice cope with metabolic challenges at high altitude.

Keywords: High-altitude hypoxia, deer mice, cardiac mitochondria, reactive oxygen species

O2k-Network Lab: CA Hamilton Scott GR


Affiliation

Saleem Ranim, Scott GR
Department of Biology, McMaster University, Hamilton, Ontario, Canada
Corresponding author: saleer4@mcmaster.ca


Labels:

Stress:Temperature, Hypoxia  Organism: Mouse  Tissue;cell: Heart  Preparation: Permeabilized tissue 



HRR: Oxygraph-2k, O2k-Fluorometer  Event: E2