Modulation of dietary fat on the toxicological effects in thymus and spleen in BALB/c mice exposed to perfluorooctane sulfonate.

Perfluorooctane sulfonate (PFOS) can cause atrophy of the immune organs in rodents, but the mechanism underlying this action is not completely understood. In this study, BALB/c mice were fed a regular (RD) or high-fat diet (HFD). They were then exposed to PFOS (0, 5, and 20mg/kg/day) for 14 days. In the RD-exposure group, body weight significantly decreased and the immune organs showed considerable atrophy. Histopathological analyses showed that the corticomedullary junction of the thymus was indistinguishable, and sinus expansion in the spleen was observed. Transmission electron microscopy (TEM) results showed that lipofuscin granules and vacuoles appeared in the thymus and spleen. Increased apoptosis of thymocytes was observed. In the HFD group, all of these phenomena were not eliminated. More serious atrophy was seen in the immune organs under TEM. Even more adipocytes were in the lobules of the thymus in the HFD 20mg/kg/day PFOS groups. Expression of the proliferator-activated receptor-alpha and interleukin-1 beta were upregulated in the thymus and spleen in all exposure groups. These results suggest that PFOS may indirectly attack the immune organs by interfering with lipid metabolism, leading to co-senescence of the thymus and spleen. These data may aid understanding of how PFOS affects the immune system.