Mild testicular hyperthermia transiently increases lipid droplet accumulation and modifies sphingolipid and glycerophospholipid acyl chains in the rat testis.

Spermatogenesis is known to be vulnerable to temperature. The aim of this study was to investigate the effects on testicular lipids of the transient germ cell loss that is induced by mild testicular hyperthermia. Adult rat testes were exposed once a day to 43 °C for 15 min for 5 days and the effects were followed for several weeks. Two week after the last heat exposure, spermatocytes and early spermatids had virtually disappeared and the seminiferous tubules were populated mostly by mature spermatids and spermatozoa. One week later, the latter were also absent and mostly Sertoli cells populated the tubules. During these 3 weeks, glycerophospholipids (Gpl) and triacylglycerols with long-chain polyunsaturated fatty acids (PUFA) (e.g., 22:5n-6) and species of sphingomyelin and ceramide with nonhydroxy and 2-hydroxy very long-chain (VLC) PUFA (e.g., 28:4n-6, 2-OH 30:5n-6) decreased alongside the germ cells. Concomitantly, the amounts of cholesteryl esters and ether-linked triglycerides increased, both lipids accumulating long-chain and very-long-chain polyenes. This concurred with a considerable buildup of lipid droplets in Sertoli cells, evidently containing these neutral lipids, apparently formed during germ cell-derived membrane lipid catabolism. Between week 4 and week 6, new cohorts of spermatocytes appeared, and by week 12 most cell changes were reversed. Accordingly, as germ cell differentiation proceeded, 22:5n-6-rich Gpl augmented and spermatocyte-associated sphingolipids with nonhydroxy VLCPUFA appeared before their 2-hydroxy counterparts. The unique fatty acids of rat testicular lipids after mild hyperthermia reveal lipid catabolic and biosynthetic reactions that occur in normal spermatogenesis.