Effects of fumonisin B1 treatment on blood-brain barrier transfer in developing rats

• Published in: Neurotoxicology and teratology Vol. 19; no. 2; pp. 151 - 155
• Main Authors: Kwon, Oh-Seung, Sandberg, Jennifer A., Slikker, William
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01.03.1997; Elsevier Science
• Subjects: Animals; Area Under Curve; Biological and medical sciences; Blood-brain barrier; Blood-Brain Barrier - drug effects; Blood-Brain Barrier - physiology; Carboxylic Acids - blood; Carboxylic Acids - toxicity; Carcinogens, Environmental - analysis; Carcinogens, Environmental - toxicity; Chromatography, High Pressure Liquid; Female; Fumonisin B1; Fumonisins; Male; Medical sciences; Mycotoxin; Pharmacokinetics; Plant poisons toxicology; Pregnancy; Prosencephalon - chemistry; Rats; Rats, Sprague-Dawley; Sphinganine; Sphingosine; Sphingosine - analogs & derivatives; Sphingosine - blood; Sphingosine - pharmacokinetics; Toxicology; Fumonisin B1; Blood-brain barrier; Pharmacokinetics; Mycotoxin; Sphinganine; Sphingosine; Toxicokinetics; Nervous system diseases; Toxicity; Sphingolipid; Blood brain barrier; Brain (vertebrata)
• ISSN: 0892-0362; 1872-9738
• DOI: 10.1016/S0892-0362(96)00217-6

Fumonisin B1 (FB1), a toxic metabolite of the fungus Fusarium moniliforme found in contaminated corn, is considered an etiologic agent of equine leukoencephalomalacia. Because FB1 exposure is associated with alteration of sphingolipid metabolism, the purpose of this study was to elucidate whether blood sphinganine (Sa) levels affect brain Sa levels. Sa and sphingosine (So) levels in brain tissue and plasma were analyzed by HPLC. Area under the curve (AUC0 → 24h) ratios of brain Sa to plasma Sa levels were about 40 after a single 0.8 or 8 mg/kg SC dose of FB1. The AUC0 → 12h ratio of brain FB1 to plasma FB1 was 0.02. The fact that FB1 alters brain Sa levels and SaSo ratios indicates that sphingolipid metabolism in the central nervous system of developing rats is vulnerable to FB1 exposure. These data support our hypothesis that alterations of the brain Sa levels are related to the direct action of FB1 on the brain rather than transport of peripheral Sa to the brain.