Both Lentinula edodes (black oak mushroom or Shiitake in Japanese) and Pleurotus ostyeatus (oyster mushroom or Hiratake) belong to the class Hymenomycetes (Basidiomycotina), and are important commercial mushrooms in Japan. In nature, these fungi inhabit dead broad-leaved trees, and they interact with various kinds of microorganisms in wood. However, little is known about the precise nature of the majority of such interactions. These fungi cause white rot of wood by first removing lignin and other amorphous wood components, followed by the degradation of exposed cellulose microfibrils. Wood is a unique substrate for microorganisms because it contains exceptionally large amounts of cellulose, hemicellulose and lignin, while water-soluble and solvent-soluble (e.g. fats, oils, waxes) and proteins occur relatively in small quantities. Therefore, wood in general is strongly deficient in nitrogen, containing less than 0.3% (w/w). Mechanisms by which wood-decay fungi manage to decay nitrogen-deficient wood are not well known.
Histopathological changes of mouse digestive tracts induced by trichothecenes were examined lightand scanning electron microscopically. Using ICR mice, acute responses up to 48 hr of the digestive tracts to the mycotoxins were demonstrated. A single dose of T-2 toxin (T-2), f usarenon-X (FX), nivalenol (NIV) and deoxynivalenol (DON) at a dose of 15.6, 10.2, 12.3 and 46 mg/kg b.w., respectively, were incubated to 4-week-old male ICR mice. In the stomach, FX caused a marked dilatation within 48 hr, while the other mycotoxins did not. Histologically, exfoliation ofepithelial cells and bacterial growth on the surface of tissue defects were seen in the glandular stomach of mice treated with T-2 and FX. FX caused necrosis and shortening of gland cells, cell infiltration in submucosa, and thinning of muscle layer most severely among the mycotoxins tested.In contrast, DON or NIV caused ulcer and cell infiltration preferentially in forestomach. In the small intestine were noted 4 processes, i.e. 1) necrosis of crypt immature cells, 2) cell infiltration in mucosa, 3) cystic change of crypt and 4) abnormal arrangement of regenerating villi. The processes 1) and 2) occurred in the treatment with FX, T-2 or DON and the processes 3) and 4) were noted only in the treatment with FX.
Chaetochromin A, a bis(naphtho-γ-pyrone) mycotoxin from Chaetomium gracile, was spectrophotometrically examined for its interactions with bovine serum albumin (BSA) and magnesium ion to gain insight into the molecular mechanism for its toxic action on mitochondria. It was found that chaetochromin A bound to anion binding site(s) of serum albumin by the electrostatic and hydrophobic interactions. Chaetochromin A showed a spectral alteration in the presence of magnesium ion, indicating a complex formation between them.
U-3 and ustiloxin A, a crude extract and a purified toxin produced by Ustilaginoidea virens, caused the histological and electron microscopic changes of apoptosis and mitoses in the liver, kidney and urinary bladder of mice when given by single or repeated intraperitoneal injections. Apoptosis occurred in the liver, urinary bladder and kidney with the peaks at 6 h, 48 h and 7 days after single injection of U-3, respectively. Repeated injections caused varied stages of apoptosis in the liver cells as revealed by electron microscopy.