Fumonisin B1 hepatotoxicity in mice is attenuated by depletion of Kupffer cells by gadolinium chloride.

摘要: Fumonisin B1 (FB1) is a toxic and carcinogenic mycotoxin produced by Fusarium verticillioides found on corn worldwide. The biological effects of FB1 are attributed to sphingolipid metabolism disruption as result ceramide synthase inhibition. Tumor necrosis factor alpha (TNFalpha) an important modulator hepatotoxicity. Kupffer cells major source cytokine production in liver. In the present study we investigated cell depletion gadolinium hepatotoxicity female BALB/c mice. Mice were given saline or 50 mg/kg chloride once via tail vein; 16 h later they treated with subcutaneous injections vehicle 2.25 mg/kg/day for three successive days. Gadolinium significantly attenuated FB1-induced increases activities circulating alanine aminotransferase aspartate reduced hepatocyte apoptosis free sphinganine accumulation Both treatments individually increased expression selected signal factors; e.g., TNFalpha, TNF receptor 1, TNF-related apoptosis-inducing ligand, lymphotoxin beta, interferon gamma, transforming growth beta1; did not alter above genes. Results indicated that play role Decreased protective TNFalpha signaling may part account its ameliorating effect liver damage.