citrinin and ferric-chloride

The inhibition by citrinin (CTN) of lipid peroxidation of mitochondria, sub-mitochondrial particles (SMP) and microsomes was studied. This effect was reversed by the presence of high concentrations of Fe3+ (0.4 and 0.5 mM), suggesting chelation of the mycotoxin with iron or interference in the reduction of Fe3+.

Topics: Animals; Chlorides; Citrinin; Drug Interactions; Female; Ferric Compounds; Iron; Lipid Peroxidation; Male; Malondialdehyde; Microsomes, Liver; Mitochondria, Liver; Rats; Rats, Wistar

Experiments with Neisseria meningitidis have shown that Fe3+ to some extent can reverse the toxicity of ochratoxin A and citrinin, as measured by inhibition zones around impregnated paper discs. Similar phenomena were observed with the less toxic ochratoxin B. Zearalenone also inhibited growth, but its effect was not counteracted by iron. The mycotoxins aflatoxin B1 and deoxynivalenol did not inhibit bacterial growth at all. Desferal (deferoxamine) also inhibited growth of meningococci, but iron totally abolished this inhibition. The results indicate that ochratoxin A and citrinin interfere with iron metabolism in this organism but that other additional toxic mechanisms are involved as well since a marked growth inhibition by both toxins was also observed in the presence of iron. One function of ochratoxin A and citrinin in nature could consequently be to affect the iron uptake of other competing microorganisms. Since both toxins interfere with iron and both cause nephropathy, a possible connection between these properties and lipid peroxidation is also briefly discussed.

Topics: Chlorides; Citrinin; Ferric Compounds; Kidney Diseases; Microbial Sensitivity Tests; Mycotoxins; Neisseria meningitidis; Ochratoxins