Amelioration of the Pulmonary Toxic Effects of 4-ipomeanol in Mice by Fermentation of Mold-damaged Sweet Potatoes

Abstract

Stressed sweet potatoes infected with mold (Fusarium sp.) produce the furanoterpenoid 4-ipomeanol, which is pneumotoxic to cattle. Mechanical injury, chill injury, chemical injury, or infection with nematodes or fungi will stress sweet potatoes to produce toxic metabolites, which are further metabolized by Fusarium sp. The most abundant toxin produced is 4-ipomeanol. Pulmonary cytochrome P450 enzymes oxidize 4-ipomeanol to reactive species that cause pulmonary damage. Most of the pulmonary cytochrome P450 is contained in non-ciliated epithelial cells (Clara cells) that line bronchioles and bronchi. Within 1 day of ingestion, affected cattle develop interstitial pneumonia that causes an acute respiratory distress syndrome (ARDS). This can result in death from asphyxiation.

The risk of ARDS prevents the sweet potato from being used as cattle feed, which is unfortunate since there is an abundance of sweet potato waste in certain regions of the United States. The sweet potato is ranked 7th as a world crop. In 1995 approximately 1.3 billion pounds of sweet potatoes were produced in the United States. North Carolina alone produced 480 million pounds. Nearly 25% of the sweet potatoes harvested (approximately 1.8 million bushels) are culled, and are either dumped in a landfill or spread on crop land. Sweet potatoes have already been shown to have nutritional value equivalent to corn. Since pneumotoxicity excludes the sweet potato from use as a dietary source in cattle, we have begun investigating processing methods that may eliminate the furanoterpenoid toxins. To date our work suggests that simple processing methods may degrade the furanoterpenoids and eliminate pneumotoxicity.