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Difference between revisions of "Figueira 2014 Abstract MiP2014"

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|year=2014
|year=2014
|event=MiP2014
|event=MiP2014
|abstract=Previous data provided evidence that isolated liver mitochondria from female rats present higher rates of resting (LEAK) and ADP-stimulated (OXPHOS) O2 consumption than from male ones [1]. Furthermore, estrogens are cytoprotective, drive mitochondrial biogenesis and may modulate mitochondrial calcium homeostasis in brain and heart in in vitro models [2,3]. It is unknown whether such gender dimorphism occurs for other mitochondrial functions or in other tissues. Therefore, we aimed to study whether mitochondrial respiration and mitochondrial calcium influx and efflux rates exhibit tissue-specific gender dimorphism.  
|abstract=Previous data provided evidence that isolated liver mitochondria from female rats present higher rates of resting ([[LEAK]]) and ADP-stimulated ([[OXPHOS]]) O<sub>2</sub> consumption than from male ones [1]. Furthermore, estrogens are cytoprotective, drive mitochondrial biogenesis and may modulate mitochondrial calcium homeostasis in brain and heart in in vitro models [2,3]. It is unknown whether such gender dimorphism occurs for other mitochondrial functions or in other tissues. Therefore, we aimed to study whether mitochondrial respiration and mitochondrial calcium influx and efflux rates exhibit tissue-specific gender dimorphism.  


Liver, skeletal muscle, heart and brain mitochondria were isolated from female and male Wistar rats by differential centrifugation. Mitochondrial respiratory states were evaluated by high-resolution respirometry. Mitochondrial calcium transport (ruthenium red-sensitive initial influx at 25 ”M external free calcium and sodium-dependent, at 15 mM sodium, and -independent efflux) was assessed by following external free calcium levels with the fluorescent probe CaGreen-5N under suitable conditions and in the presence of inhibitors of mitochondrial permeability transition. In isolated male mitochondria O2 fluxes (mean±SD nmol∙min-1∙mg-1) for OXPHOS and LEAK respectively, were: 37.6±9.8 and 8.6±2.6 in liver, 106.1±24.7 and 12.8±3.4 in skeletal muscle, 137.1±42.1 and 25.9±4.7 in heart, and 31.1±8.2 and 4.8±1.3 in brain. Calcium influx and sodium-dependent efflux respectively, were (mean±SD nmol∙min-1∙mg-1): 228.6±77.1 and 0.69±0.39 in liver, 56.12±20.5 and 3.31±0.67 in skeletal muscle, 39.4±18.6 and 8.25±1.42 in heart, and 54.6±23.9 and 2.25±0.89 in brain from males. Among the assessed respiratory and calcium transport variables, the only statistically significant (P<0.05) difference between genders occurred for liver mitochondrial O2 OXPHOS capacity, which was 15% higher in female than in male rats.
Liver, skeletal muscle, heart and brain mitochondria were isolated from female and male Wistar rats by differential centrifugation. Mitochondrial respiratory states were evaluated by high-resolution respirometry. Mitochondrial calcium transport (ruthenium red-sensitive initial influx at 25 ”M external free calcium and sodium-dependent, at 15 mM sodium, and -independent efflux) was assessed by following external free calcium levels with the fluorescent probe CaGreen-5N under suitable conditions and in the presence of inhibitors of mitochondrial permeability transition. In isolated male mitochondria O<sub>2</sub> fluxes (mean±SD nmol∙min<sup>-1</sup>∙mg<sup>-1</sup>) for OXPHOS and LEAK respectively, were: 37.6±9.8 and 8.6±2.6 in liver, 106.1±24.7 and 12.8±3.4 in skeletal muscle, 137.1±42.1 and 25.9±4.7 in heart, and 31.1±8.2 and 4.8±1.3 in brain. Calcium influx and sodium-dependent efflux respectively, were (mean±SD nmol∙min<sup>-1</sup>∙mg<sup>-1</sup>): 228.6±77.1 and 0.69±0.39 in liver, 56.12±20.5 and 3.31±0.67 in skeletal muscle, 39.4±18.6 and 8.25±1.42 in heart, and 54.6±23.9 and 2.25±0.89 in brain from males. Among the assessed respiratory and calcium transport variables, the only statistically significant (''P''<0.05) difference between genders occurred for liver mitochondrial OXPHOS capacity, which was 15% higher in female than in male rats.


We conclude that gender dimorphisms for the mitochondrial functions evaluated here is tissue-specific and is confined to higher maximal ADP-stimulated respiration in isolated liver mitochondria from female rats.
We conclude that gender dimorphisms for the mitochondrial functions evaluated here is tissue-specific and is confined to higher maximal ADP-stimulated respiration in isolated liver mitochondria from female rats.

Revision as of 14:43, 9 August 2014

Mitochondrial respiration and calcium transport in rat tissues: conversely from skeletal muscle, heart and brain, isolated liver mitochondria exhibit gender dimorphism in respiratory activity.

Link:

MiP2014, Book of Abstracts Open Access

Figueira TR, Chweih H, Castilho RF (2014)

Event: MiP2014

Previous data provided evidence that isolated liver mitochondria from female rats present higher rates of resting (LEAK) and ADP-stimulated (OXPHOS) O2 consumption than from male ones [1]. Furthermore, estrogens are cytoprotective, drive mitochondrial biogenesis and may modulate mitochondrial calcium homeostasis in brain and heart in in vitro models [2,3]. It is unknown whether such gender dimorphism occurs for other mitochondrial functions or in other tissues. Therefore, we aimed to study whether mitochondrial respiration and mitochondrial calcium influx and efflux rates exhibit tissue-specific gender dimorphism.

Liver, skeletal muscle, heart and brain mitochondria were isolated from female and male Wistar rats by differential centrifugation. Mitochondrial respiratory states were evaluated by high-resolution respirometry. Mitochondrial calcium transport (ruthenium red-sensitive initial influx at 25 ”M external free calcium and sodium-dependent, at 15 mM sodium, and -independent efflux) was assessed by following external free calcium levels with the fluorescent probe CaGreen-5N under suitable conditions and in the presence of inhibitors of mitochondrial permeability transition. In isolated male mitochondria O2 fluxes (mean±SD nmol∙min-1∙mg-1) for OXPHOS and LEAK respectively, were: 37.6±9.8 and 8.6±2.6 in liver, 106.1±24.7 and 12.8±3.4 in skeletal muscle, 137.1±42.1 and 25.9±4.7 in heart, and 31.1±8.2 and 4.8±1.3 in brain. Calcium influx and sodium-dependent efflux respectively, were (mean±SD nmol∙min-1∙mg-1): 228.6±77.1 and 0.69±0.39 in liver, 56.12±20.5 and 3.31±0.67 in skeletal muscle, 39.4±18.6 and 8.25±1.42 in heart, and 54.6±23.9 and 2.25±0.89 in brain from males. Among the assessed respiratory and calcium transport variables, the only statistically significant (P<0.05) difference between genders occurred for liver mitochondrial OXPHOS capacity, which was 15% higher in female than in male rats.

We conclude that gender dimorphisms for the mitochondrial functions evaluated here is tissue-specific and is confined to higher maximal ADP-stimulated respiration in isolated liver mitochondria from female rats.


‱ O2k-Network Lab: BR Campinas Vercesi AE


Labels: MiParea: Respiration, Gender 

Stress:Permeability transition  Organism: Rat  Tissue;cell: Heart, Skeletal muscle, Nervous system, Liver  Preparation: Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property. 

Regulation: Calcium 


HRR: Oxygraph-2k 

MiP2014 

Affiliation

Dep Clinical Pathology, Fac Medical Sc, State Univ Campinas, SĂŁo Paulo, Brazil. - [email protected]

References

  1. Justo R, Boada J, Frontera M, Oliver J, BermĂșdez J, Gianotti M (2005) Gender dimorphism in rat liver mitochondrial oxidative metabolism and biogenesis. Am J Physiol Cell Physiol 289: 372-8.
  2. Morkuniene R, Arandarcikaite O, Ivanoviene L, Borutaite V (2010) Estradiol-induced protection against ischemia-induced heart mitochondrial damage and caspase activation is mediated by protein kinase G. Biochim Biophys Acta 1797: 1012-7.
  3. Nilsen J, Brinton RD (2003) Mechanism of estrogen-mediated neuroprotection: regulation of mitochondrial calcium and Bcl-2 expression. Proc Natl Acad Sci U S A 100: 2842-7.