Fumonisins are mycotoxins produced by Fusarium moniliforme, F. proliferatum, and related Fusnarium species found on corn. They occur naturally in corn-based feeds and foods and are suspected human esophageal carcinogens. Fumonisin B(1) (FB(1)), the most common homologue, causes the animal diseases associated with F: moniliforme. Hepato- and nephrotoxicities, disrupted sphingolipid metabolism, and liver cancer have been found in rats fed FB1. To determine the in vivo effects of diets containing fumonisins B(2) (FB(2)) or B(3) (FB(3)), male rats were fed culture materials (CM) of FB(1) non-producing F. moniliforme isolates to provide low (4.6-6.7 ppm), mid (32-49 ppm) or high (219-295 ppm) dietary levels of either FB(2) (FB(2)CM) or FB(3) (FB(3)CM). Other groups were fed culture material of an FBI producing isolate (FB(1)CM) providing 6.9, 53 or 303 ppm total fumonisins (FB1 FB(2) : FB(3) = 1.0 : 0.38 : 0.15) and a tenth group was fed a control diet having no detectable fumonisins. One-half (n = 5/group) the animals were killed after three weeks, at which time the toxicological and histopathological effects of the three culture materials were similar, mimicked the effects of FBI, and included decreased body weight gains, serum chemical indicators of hepatotoxicity, decreased kidney weights, and apoptosis of hepatocytes and kidney tubular epithelium. FB(1)CRM, FB(2)CM, and FB(3)CM affected sphingolipids, causing increased sphinganine to sphingosine ratios (Sa/So) in both liver and kidneys. The remaining animals (n = 5/group) were fed a control diet for three additional weeks. All body weight and tissue specific effects, including increased Sa/So, induced by the FB2CM, FB3CM and low level FB(1)CM diets were absent following the recovery period. Except for mild biliary lesions found in the high dose FB(1)CM group and a few apoptotic hepatocytes present in one mid- and two high-dose FB(1)CM rats, no evidence of toxicity remained in these groups following the recovery period.