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Diacetoxyscirpenol and deoxynivalenol, two trichothecene mycotoxins shown previously to exert immunosuppressive effects on the immune system were examined for their in vitro effects on some functions of murine peritoneal macrophages. The cells were pre-incubated for 4 hr with the mycotoxin concentrations of 0.1 ng/ml-1 micrograms/ml. At concentrations that did not affect the cell viability (Specific Lactate Dehydrogenase test), diacetoxyscirpenol and deoxynivalenol suppress microbicidal activity of phagocytic cells. The diacetoxyscirpenol concentrations, which reduce phagocytosis (2 ng/ml), microbicidal activity (1 ng/ml), superoxide anion production (1 ng/ml) and phagosome-lysosome fusion (0.1 ng/ml), indicate that the inhibition of killing mechanism arise from both oxidative and non-oxidative pathways. Phagocytosis, microbicidal activity and superoxide anion production are inhibited by deoxynivalenol at 1 ng/ml whereas phagosome-lysosome fusion is reduce above 100 ng/ml. These results suggest that microbicidal activity inhibition by deoxynivalenol did not depend on non-oxidative pathway (phagosome-lysosome fusion) impairment.

Mice receiving patulin (10 mg/kg) from 1 to 4 days showed enhancing resistance to intraperitoneal challenge with 10(8) viable Candida albicans at day 2. Resistance to C. albicans infection (10(6) blastospores) appeared to be unchanged after cyclophosphamide oral administration (60 mg/kg). Immunoglobulins levels (IgA, IgM, IgG) are marked depressed (10 to 75%) in mice infected and/or treated by patulin and cyclophosphamide. The results show that an increase of neutrophil count may be among the factor underlying the late increase in resistance to C. albicans after administration of patulin.

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