“Trilongins” Offer Insight into Mold Toxicity

Mold contamination inside buildings is a widespread occurrence that can cause a range of adverse health effects in certain people. But with tens of thousands of mold species and many mechanisms through which they may cause harm, much remains unknown about this realm of environmental exposures. Investigators now report that one mold, Trichoderma longibrachiatum, does some of its damage through a combined set of toxins previously unidentified for this species, at least two of which also had never been identified for any fungal species. 3 The team of Finnish, Hungarian, and Russian researchers also determined that two classes of the toxin act synergistically to exacerbate the potency and duration of the toxic effects. They are unaware of any previous reports of such synergy. Each mold species produces a unique set of toxins depending on species, strain, and growing conditions (e.g., temperature, incubation time, nutrient source, associated substances), with some uncertainty continuing to occur as toxin identification science is refined, according to principal investigator Mirja Salkinoja-Salonen, research director for the Department of Food and Environmental Sciences at Finland's University of Helsinki. T. longibrachiatum, a fungus commonly found around the globe in a variety of damp indoor and outdoor settings, has been identified in a handful of case reports as an emerging human pathogen implicated in allergic sinusitis, lung and skin infections, and fatal postoperative infections in immunocompromised patients. In the current study the researchers began by exposing boar sperm cells to T. longibrachiatrum isolates taken from inside a Finnish moisture-damaged home, from the bodies of people with serious T. longibra-chiatum infections, and from three diverse terrestrial locations (Wales, Egypt, and Antarctica). Exposure to T. longibrachiatum was linked to increased permeability, via voltage-dependent sodium and potassium ion channels, in some sperm cellular membranes. Additional observed damage, generally consistent with other research, included sperm motility inhibition and mitochondrial depolarization. Normal ion channels perform vital cellular functions such as electrical and chemical signaling, regulation of cytoplasmic or vesicular ion concentration and pH, and cell volume regulation. They also maintain mitochondrial polarization, which is essential to the production of adenosine triphosphate (ATP), the molecule that acts as the medium of energy exchange for all cells. Dysfunctional ion channels are known to be key elements in a panoply of diseases, 4 Further investigation by the team revealed that the substances involved in the ion channel damage contained various mixtures of two size classes of peptaibols—one 11-residue …