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Tumor Necrosis Factor--Stimulated Lactate Production Is Linked to Lactate Dehydrogenase A Expression and Activity Increase in Porcine Cultured Sertoli Cells¹

INSERM U-407, Communications Cellulaires en Biologie de la Reproduction, Centre Hospitalier Lyon-Sud, Pierre-Benite, France

Address all correspondence and requests for reprints to: Dr. M. Benahmed, INSERM U-407, Communications Cellulaires en Biologie de la Reproduction, Bât 3 B, Centre Hospitalier Lyon-Sud, 69 495 Pierre-Benite, France.

By using, as a model, cultured testicular immature Sertoli cells, the action of tumor necrosis factor- (TNF) and the site of action of the cytokine on lactate production were studied. TNF stimulated in a time- and dose-dependent manner (with an ED₅₀ of 0.1 nM) Sertoli cell lactate production. Two major sites involved in TNF action were identified. Firstly, TNF was shown to increase the uptake of glucose substrate in a time- and dose-dependent manner. The maximal effect was observed after 24 h of treatment, with an ED₅₀ of 0.1 nM. Secondly, TNF increased the activity of lactate dehydrogenase (LDH) A isoform, which is involved in the conversion of pyruvate into lactate. This increase in LDH-A activity was detected at 12 h and was maximal after 24 h of treatment with TNF. The stimulatory effect of the cytokine on the LDH-A isoform was observed with an ED₅₀ of 0.05 nM. Such an increase in LDH-A activity was related to an increase in LDH-A expression, because TNF stimulated LDH-A messenger RNA (size, 1.5 kilobases, determined by Northern blotting analysis). Together, assuming that in the seminiferous tubules, TNF is produced by spermatids that use lactate for their energetic metabolism, we suggest that the cytokine may potentially represent a signal used by germ cells to enhance lactate production in Sertoli cells through, at least, a redistribution of LDH isoforms in favor of LDH-A.

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