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Research in veterinary science1997; 62(2); 93-97; doi: 10.1016/s0034-5288(97)90127-2

Oxidative energy metabolism in equine tendon cells.

Abstract: Hypoxia has been suggested as a possible cause of tissue degeneration and subsequent rupture in equine tendons. To determine whether low oxygen tension is likely to be detrimental to tendon cell function, experiments were designed to investigate oxidative energy metabolism in freshly isolated and cultured equine tendon cells. Freshly isolated tenocytes and cultured fibroblasts possessed activities of the mitochondrial enzyme citrate synthase similar to those of other mammalian cells, with well defined oxidative metabolism. D-[6(-14)C]-glucose oxidation was measurable in both freshly isolated and explant-derived cells. The content of adenosine triphosphate (ATP) in cultured cells was decreased by incubation with a mitochondrial respiratory uncoupler. These data demonstrate that tendon cells are capable of oxidative energy metabolism and rely upon it to maintain cellular ATP levels. Hypoxia must therefore be considered as a possible factor leading to tendon degeneration and subsequent injury.
Publication Date: 1997-03-01 PubMed ID: 9243704DOI: 10.1016/s0034-5288(97)90127-2Google Scholar: Lookup
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  • Journal Article
  • Research Support
  • Non-U.S. Gov't

Summary

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This research paper investigates the role hypoxia, or low oxygen levels, may play in equine tendon degeneration and potential rupture, specifically looking at oxidative energy metabolism in tendon cells. It suggests that tendon cell function can be affected under low oxygen conditions, adding to the body of research around hypoxia as a cause of equine tendon degeneration.

Understanding Oxidative Energy Metabolism

  • The study first lays a foundation around oxidative energy metabolism. This refers to the biochemical process by which cells process glucose and oxygen to generate energy in the form of adenosine triphosphate (ATP).
  • The researchers report that tendon cells in horses (freshly isolated and cultured) display similar characteristics to other mammalian cells when it comes to oxidative metabolism, demonstrating that they are capable of this process.
  • The enzyme citrate synthase, key to oxidative metabolism, was found in comparable levels in these tendon cells. These levels were not affected by whether the cells were freshly isolated or cultured.

Role of Glucose Oxidation and ATP

  • The study measures the oxidation of D-[6(-14)C]-glucose, a radioactively marked version of glucose in both freshly isolated and explant-derived cells. This demonstrates the ongoing process of oxidative metabolism within these cells.
  • ATP, the ‘energy currency’ produced by oxidative metabolism, saw a decrease in cultured cells when these were subjected to a mitochondrial respiratory uncoupler. This emphasizes the dependence of these cells on oxidative metabolism to maintain cellular energy through ATP.

Implications for Tendon Health

  • Given this reliance on oxidative metabolism, the study hypothesizes that hypoxia or low oxygen conditions could adversely affect tendon health.
  • Under such conditions, the function of tendon cells could be compromised as their capability to maintain energy levels through oxidative energy metabolism is hindered.
  • This could become a contributing factor towards tendon degeneration and injury in horses, making hypoxia a critical point of consideration in efforts aimed at safeguarding the health of equine tendons.

Cite This Article

APA
Birch HL, Rutter GA, Goodship AE. (1997). Oxidative energy metabolism in equine tendon cells. Res Vet Sci, 62(2), 93-97. https://doi.org/10.1016/s0034-5288(97)90127-2

Publication

ISSN: 0034-5288
NlmUniqueID: 0401300
Country: England
Language: English
Volume: 62
Issue: 2
Pages: 93-97

Researcher Affiliations

Birch, H L
  • Royal Veterinary College, Hawkshead Lane, North Mymms, Hatfield.
Rutter, G A
    Goodship, A E

      MeSH Terms

      • Adenosine Diphosphate / analysis
      • Adenosine Diphosphate / metabolism
      • Adenosine Triphosphate / analysis
      • Adenosine Triphosphate / metabolism
      • Animals
      • Carbon Radioisotopes
      • Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone / pharmacology
      • Cells, Cultured
      • Citrate (si)-Synthase / analysis
      • Citrate (si)-Synthase / metabolism
      • Citrate (si)-Synthase / physiology
      • Energy Metabolism / physiology
      • Fibroblasts / enzymology
      • Glucose / metabolism
      • Glycolysis / physiology
      • Horse Diseases / metabolism
      • Horse Diseases / physiopathology
      • Horses / metabolism
      • Horses / physiology
      • Hypoxia / metabolism
      • Hypoxia / physiopathology
      • Hypoxia / veterinary
      • L-Lactate Dehydrogenase / analysis
      • L-Lactate Dehydrogenase / metabolism
      • L-Lactate Dehydrogenase / physiology
      • NAD / metabolism
      • Oxidation-Reduction
      • Oxygen Consumption / physiology
      • Tendons / cytology
      • Tendons / enzymology
      • Tendons / metabolism
      • Time Factors
      • Uncoupling Agents / pharmacology

      Citations

      This article has been cited 11 times.
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      2. Thankam FG, Chandra IS, Kovilam AN, Diaz CG, Volberding BT, Dilisio MF, Radwan MM, Gross RM, Agrawal DK. Amplification of Mitochondrial Activity in the Healing Response Following Rotator Cuff Tendon Injury. Sci Rep 2018 Nov 19;8(1):17027.
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      9. Simonin MA, Gegout-Pottie P, Minn A, Gillet P, Netter P, Terlain B. Pefloxacin-induced achilles tendon toxicity in rodents: biochemical changes in proteoglycan synthesis and oxidative damage to collagen. Antimicrob Agents Chemother 2000 Apr;44(4):867-72.
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      10. Tamburro MK, Bonilla KA, Shetye SS, Leahy TP, Eekhoff JD, Kim MS, Petucci C, Tobias JW, Farber DC, Soslowsky LJ. Moderate- and High-Speed Treadmill Running Exercise Have Minimal Impact on Rat Achilles Tendon. J Orthop Res 2025 Mar;43(3):519-530.
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      11. Liang W, Zhou C, Deng Y, Fu L, Zhao J, Long H, Ming W, Shang J, Zeng B. The current status of various preclinical therapeutic approaches for tendon repair. Ann Med 2024 Dec;56(1):2337871.
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