ToxSci Advance Access originally published online on December 1, 2004
Toxicological Sciences 2005 84(1):186-194; doi:10.1093/toxsci/kfi045
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Toxicological Sciences vol. 84 no. 1 © Society of Toxicology 2005; all rights reserved.
Stachybotrys chartarum Alters Surfactant-Related Phospholipid Synthesis and CTP:Cholinephosphate Cytidylyltransferase Activity in Isolated Fetal Rat Type II Cells
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* Departments of Oral Biology and Human Anatomy and Cell Science, Faculties of Dentistry & Medicine, University of Manitoba, Winnipeg, Manitoba, Canada R3E0W2; Department of Biology, St. Mary's University, Halifax, Nova Scotia B3H3C3, Canada; National Research Council, Institute for Biodiagnostics, Winnipeg, Canada R3B1Y6; ¶ Health Canada, Health Products and Food Branch, Winnipeg, Manitoba, Canada A2J3Y1; and || Manitoba Institute of Child Health, Biology of Breathing Group, Children's Hospital Foundation, Winnipeg, Manitoba, Canada R3E3P4
Received September 19, 2004; accepted November 17, 2004
Stachybotry chartarum, a fungal contaminant of water-damaged buildings commonly grows on damp cellulose-containing materials. It produces a complex array of mycotoxins. Their mechanisms of action on the pulmonary system are not entirely clear. Previous studies suggest spore products may depress formation of disaturated phosphatidylcholine (DSPC), the major surface-active component of pulmonary surfactant (PS). If S. chartarum can indeed affect formation of this phospholipid, then mold exposure may be a significant issue for pulmonary function in both mature lung and developing fetal lung. To address this possibility, fetal rat type II cells, the principal source of DSPC, were used to assess effects of S. chartarum extract on formation of DSPC. Isolated fetal rat lung type II cells prelabeled with 3H-choline and incubated with spore extract showed decreased incorporation of 3H-choline into DSPC. The activity of CTP:cholinephosphate cytidylyltransferase (CPCT), the rate-limiting enzyme in phosphatidylcholine synthesis was reduced by approximately 50% by a 1:10 dilution of spore extract. Two different S. chartarum extracts (isolates from S. chartarum (Cleveland) and S. chartarum (Hawaiian)) were used to compare activity of CPCT in the presence of phosphatidylglycerol (PG), a known activator. PG produced an approximate two-fold increase in CPCT activity. The spore isolate from Hawaii did not alter enzyme activity. S. chartarum (Cleveland) eliminated the PG-induced activation of CPCT. These results support previous observations that mold products alter PS metabolism and may pose a risk in developing lung, inhibiting surfactant synthesis. Different isolates of the same species of fungus are not equivalent in terms of potential exposure risks.
Key Words: lung; mold spores; cytidylyltransferase; surfactant.
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