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Cell biology international2007; 31(9); 878-886; doi: 10.1016/j.cellbi.2007.02.002

Oxygen consumption of equine articular chondrocytes: Influence of applied oxygen tension and glucose concentration during culture.

Abstract: We investigated the oxygen (O(2)) uptake of equine articular chondrocytes to assess their reactions to anoxia/re-oxygenation. They were cultured under 5% or 21% gas phase O(2) and at glucose concentrations of 0, 1.0 or 4.5g/L in the culture medium (n=3). Afterwards, the O(2) consumption rate of the chondrocytes was monitored (oxymetry) before and after an anoxia period of 25min. The glucose consumption and lactate release were measured at the end of the re-oxygenation period. The chondrocytes showed a minimal O(2) consumption rate, which was hardly changed by anoxia. Independently from the O(2) tension, glucose uptake by the cells was about 30% of the available culture medium glucose, thus higher for cells at 4.5g/L glucose (n=3). Lactate release was also independent from O(2) tension, but lower for cells at 4.5g/L glucose (n=3). Our observations indicated that O(2) consumption by equine chondrocytes was very low despite a functional mitochondrial respiratory chain, and nearly insensitive to anoxia/re-oxygenation. But the chondrocytes metabolism was modified by an excess of O(2) and glucose.
Publication Date: 2007-02-25 PubMed ID: 17442596DOI: 10.1016/j.cellbi.2007.02.002Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

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This research aims to understand how horse cartilage cells (or equine articular chondrocytes) consume oxygen and react to periods of anoxia (oxygen deprivation) and subsequent re-oxygenation. Additionally, the impact of different oxygen and glucose levels in the culture medium on these cells is examined.

Study Design and Procedures

  • The scientists cultured equine articular chondrocytes (cartilage cells) under two different oxygen conditions—5% and 21%—and with three varying glucose concentrations (0, 1.0 or 4.5g/L) in the culture medium.
  • They applied an anoxia (oxygen deprivation) period of 25 minutes to the cultures and then used oxymetry, a process to measure the rate of oxygen consumption, to determine how the chondrocytes respond before and after this period.
  • They also measured the glucose consumption and lactate release of the cells at the end of the re-oxygenation phase.

Oxygen Consumption Findings

  • The equine chondrocytes showed a minimal rate of oxygen consumption, which remained largely unchanged throughout the period of oxygen deprivation.
  • This demonstrated the surprising resilience of these cells to variations in oxygen supply – they appeared functionally indifferent to anoxia and re-oxygenation, despite possessing a functioning mitochondrial respiratory chain (responsible for oxygen-dependent energy production).

Glucose Metabolism and Lactate Release

  • Irrespective of the oxygen tension (level of oxygen supply), the cells consumed about 30% of the available glucose in the medium. This means that cells cultured at a higher glucose concentration (4.5g/L) ended up consuming more glucose.
  • The amount of lactate (a byproduct of glucose metabolism) released by the cells was unaffected by changes in oxygen supply. However, cells cultured at a higher glucose concentration tended to release less lactate.

Conclusion

  • In conclusion, the study revealed that equine chondrocytes have a low oxygen consumption rate and are resilient to periods of oxygen deprivation and re-oxygenation.
  • The researchers also found that the metabolism of these cells was affected by excessive oxygen and glucose supply, contrary to the initial presumption that higher oxygen and glucose levels in the culture medium would increase oxygen consumption and glucose metabolism.

Cite This Article

APA
Schneider N, Mouithys-Mickalad A, Lejeune JP, Duyckaerts C, Sluse F, Deby-Dupont G, Serteyn D. (2007). Oxygen consumption of equine articular chondrocytes: Influence of applied oxygen tension and glucose concentration during culture. Cell Biol Int, 31(9), 878-886. https://doi.org/10.1016/j.cellbi.2007.02.002

Publication

ISSN: 1065-6995
NlmUniqueID: 9307129
Country: England
Language: English
Volume: 31
Issue: 9
Pages: 878-886

Researcher Affiliations

Schneider, Nicole
  • Centre of Oxygen Research & Development (CORD), Institut de Chimie, B6a, Sart Tilman, University of Liège, 4000 Liège, Belgium. ni.schneider@gmx.net
Mouithys-Mickalad, Ange
    Lejeune, Jean-Philippe
      Duyckaerts, Claire
        Sluse, Francis
          Deby-Dupont, Ginette
            Serteyn, Didier

              MeSH Terms

              • Alginates / metabolism
              • Animals
              • Cartilage, Articular / cytology
              • Cartilage, Articular / drug effects
              • Cell Count
              • Cell Culture Techniques
              • Cell Separation
              • Cell Survival / drug effects
              • Cells, Cultured
              • Chondrocytes / drug effects
              • Chondrocytes / metabolism
              • Electron Transport Complex IV / metabolism
              • Glucose / pharmacology
              • Glucuronic Acid / metabolism
              • Hexuronic Acids / metabolism
              • Horses
              • Lactic Acid / biosynthesis
              • Microspheres
              • Oxygen / pharmacology
              • Oxygen Consumption / drug effects

              Citations

              This article has been cited 8 times.
              1. Bartell LR, Fortier LA, Bonassar LJ, Szeto HH, Cohen I, Delco ML. Mitoprotective therapy prevents rapid, strain-dependent mitochondrial dysfunction after articular cartilage injury. J Orthop Res 2020 Jun;38(6):1257-1267.
                doi: 10.1002/jor.24567pubmed: 31840828google scholar: lookup
              2. Delco ML, Bonnevie ED, Szeto HS, Bonassar LJ, Fortier LA. Mitoprotective therapy preserves chondrocyte viability and prevents cartilage degeneration in an ex vivo model of posttraumatic osteoarthritis. J Orthop Res 2018 Feb 22;.
                doi: 10.1002/jor.23882pubmed: 29469223google scholar: lookup
              3. Delco ML, Bonnevie ED, Bonassar LJ, Fortier LA. Mitochondrial dysfunction is an acute response of articular chondrocytes to mechanical injury. J Orthop Res 2018 Feb;36(2):739-750.
                doi: 10.1002/jor.23651pubmed: 28696002google scholar: lookup
              4. Li J, Dong S. The Signaling Pathways Involved in Chondrocyte Differentiation and Hypertrophic Differentiation. Stem Cells Int 2016;2016:2470351.
                doi: 10.1155/2016/2470351pubmed: 28074096google scholar: lookup
              5. Rufino AT, Rosa SC, Judas F, Mobasheri A, Lopes MC, Mendes AF. Expression and function of K(ATP) channels in normal and osteoarthritic human chondrocytes: possible role in glucose sensing. J Cell Biochem 2013 Aug;114(8):1879-89.
                doi: 10.1002/jcb.24532pubmed: 23494827google scholar: lookup
              6. Yodmuang S, Gadjanski I, Chao PH, Vunjak-Novakovic G. Transient hypoxia improves matrix properties in tissue engineered cartilage. J Orthop Res 2013 Apr;31(4):544-53.
                doi: 10.1002/jor.22275pubmed: 23203946google scholar: lookup
              7. Rosa SC, Gonçalves J, Judas F, Mobasheri A, Lopes C, Mendes AF. Impaired glucose transporter-1 degradation and increased glucose transport and oxidative stress in response to high glucose in chondrocytes from osteoarthritic versus normal human cartilage. Arthritis Res Ther 2009;11(3):R80.
                doi: 10.1186/ar2713pubmed: 19490621google scholar: lookup
              8. Gibson JS, Milner PI, White R, Fairfax TP, Wilkins RJ. Oxygen and reactive oxygen species in articular cartilage: modulators of ionic homeostasis. Pflugers Arch 2008 Jan;455(4):563-73.
                doi: 10.1007/s00424-007-0310-7pubmed: 17849146google scholar: lookup