**3.1 Fungi**

Ochratoxin A is produced by *Aspergillus* and *Penicillium* species listed in Table 3. These microorganisms differ according to the ecological conditions and commodities that characterize different geographical regions. In general, *Penicillium verrucosum* is responsible for OTA contamination in cool-temperate conditions, whereas *Aspergillus ochraceus* is particularly relevant in hot-tropical regions (Battaccone et al., 2010; Scudamore, 2005).

The major *Aspergillus* producers in food and feeds are *A. alliaceus*, *A. carbonarius*, *A. ochraceus*, *A. steynii* and *A. westerdijkiae*. *A. melleus*, *A. ostianus*, *A. persii* and *A. petrakii* may produce trace amounts of OTA, but since the publication by Ciegler (1972) and Hesseltine et al. (1972) no further confirmation has been found.

In the genus *Penicillium*, *P. verrucosum* and *P. nordicum* are the only species that are able to produce OTA (Abruhnosa et al., 2010; El Khoury & Atoui, 2010). *P. chrysogenum*, *P. brevicompactum*, *P. crustosum*, *P. olsonii* and *P. oxalicum* have been claimed as OTA producers, but a confirmation of these findings is required (Paterson, 2006).


Table 3. OTA producing fungi (Abrunhosa et al., 2010; El Khoury & Atoui, 2010; Moss, 2002b).

**3.3 Toxicity** 

Weidenbach, 2002).

**4. Trichothecenes** 

of the tested animal (El Khoury & Atoui, 2010).

reach the neural tissue (Soleas et al., 2001).

OTA can have several effects, such as nephrotoxic, hepatotoxic, neurotoxic, teratogenic and immunotoxic effects on several species of animals, and can cause kidney and liver tumours in mice and rats; OTA toxicity varies depending on the sex, the species and the cellular type

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Nephropathy is the main toxic effect of OTA; it is potentially nephrotoxic in all nonruminant mammals (Ribelin et al., 1978). OTA plays an important role in the etiology of porcine nephropathy (Elling et al., 1985). This mycotoxin was also associated with human nephropathy and it is suspected to be the cause of the human Balkan Endemic Nephropathy (BEN) and the Tunisian Nephropathy (TCIN) (Hassen et al., 2004; Pfohl-Leszkowicz, 2009). The administration of OTA at gestation period in rats induced many malformations in the central nervous system. OTA can be regarded as a possible cause of certain lesions as well as damage at the cerebral level. OTA seems to be highly toxic for the nervous cells and able to

OTA is a potent teratogen for laboratory animals. It can cross the placenta and accumulate in fetal tissue, causing various morphological anomalies. It has been reported to elicit prenatal dysmorphogenesis in rats, mice, hamsters and chick embryos (El Khoury & Atoui, 2010). OTA also has an immunosuppressor effect. Necroses of lymphoid tissues has been reported, and humoral and cellular immunity affections have also been described (Creppy et al., 1991; Holmberg et al., 1988). OTA seems to play a role in the inhibition of proliferation of the peripheral T and B lymphocytes and stops the production of interleukin 2 (IL2) and its receptors (Lea et al., 1989). Moreover, it blocks the activity of killer cells as well as the production of interferon (Pfohl-Leszkowicz & Castegnaro, 1999). OTA is taken as an important immunosupressor agent, in fact it is considered to be the cause of lymphopenia, regression of the thymus, and suppression of the immunity response (Petzinger &

OTA is anticipated to be a human carcinogen based on sufficient evidence of carcinogenicity in experimental animals. Hepatocellular tumors, renal cell tumors, hepatomas, and hyperplastic hepatic nodules have been observed in male mice (Huff et al., 1992). OTA has been correlated with hepatocellular and renal-cell carcinomas and adenomas in mice and rats (El Khoury & Atoui, 2010). On the other hand there are no adequate studies of the relationship between exposure to OTA and human cancer; incidence and mortality from urothelial urinary tract tumours have been correlated with the geographical distribution of

Trichothecin was first isolated from *Trichothecium roseum* and described by Freeman and Morrison in 1949. The discovery of trichothecin was followed by the isolation and description of other trichothecenes (TCTs), such as diacetoxyscirpenol (DAS), T-2 toxin (T-

The Alimentary Toxic Aleukia (ATA) that occurred in Russia during World War II was caused by T-2 toxin and its derivatives; *F. sporotrichioides* was isolated from contaminated grains (Yazar & Omurtag, 2008). DON is the most prevalent toxin associated with Fusarium Head Blight (FHB), and it belongs to the phytotoxic type B trichothecene (Foroud & Eudes, 2009). TCTs are the most important group of mycotoxins and they are produced above all by various *Fusarium* plant pathogen species (Kimura et al., 2007). They are non-volatile, low-

Balkan endemic nephropathy in Bulgaria and Yugoslavia (Feier & Tofana, 2009).

2), nivalenol (NIV) and deoxynivalenol (DON) (Yazar & Omurtag, 2008).
