OXIDATIVE ENERGY-METABOLISM IN EQUINE TENDON CELLS

Hypoxia has been suggested as a possible cause of tissue degeneration and subsequent rupture in equine tendons. To determine whether low oxy gen tension is likely to be detrimental to tendon cell function, exper iments were designed to investigate oxidative energy metabolism in fre shly isolated and cultured equine tendon cells. Freshly isolated tenoc ytes and cultured fibroblasts possessed activities of the mitochondria l enzyme citrate synthase similar to those of other mammalian cells, w ith well defined oxidative metabolism, D-[6-C-14]-glucose oxidation wa s measurable in both freshly isolated and explant-derived cells. The c ontent 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 metaboli sm and rely upon it to maintain cellular ATP levels. Hypoxia must ther efore be considered as a possible factor leading to tendon degeneratio n and subsequent injury.