Since ZEA is a potent toxin and may cause a risk to animal and human health, it is important to investigate the acute harmful effects Tacrolimus nmr of this mycotoxin. In the present study we showed that acute ZEA administration caused deleterious hematologic effects (Fig. 1) and drastically reduced the number and motility of live spermatozoa (Fig. 2) in male Swiss albino mice. The role of oxidative stress in the toxic effects of ZEA was also investigated. Interestingly, this mycotoxin decreased GST activity in the testes and kidney (Fig. 5B–C), increased SOD activity in the liver, kidney and testes (Fig. 4A–C), and increased CAT activity in the kidney

(Fig. 3B). Intracellular accumulation of reactive oxygen species can arise from toxic insults and can perturb the cell’s natural Doramapimod molecular weight antioxidant defense system resulting in damage to all major classes of biological macromolecules. During the last decades, the oxidative stress has been pointed out as major component of several biological and pathological processes like aging, inflammation, carcinogenesis and several other diseases (Halliwell and Gutteridge, 1999). Additionally, some reports suggest that oxidative stress is a key determinant of ZEA induced toxicity in vivo and in vitro ( Abid-Essefi et al., 2009, 2011; Ben Salah-Abbes et al., 2008; Hassen et al., 2007; Salah-Abbes et al., 2009a). In this context,

both enzymatic and non-enzymatic antioxidant defenses are fundamental to prevent oxidative stress and may also indicate the level of protection against foreign agents. In the present study, we found that acute ZEA treatment significantly increased catalase activity in the kidney and SOD activity in the liver, kidney and testes, suggesting compensatory increases in antioxidant enzyme activity in attempt to prevent oxidative damage to cells and macromolecules. In this context, such assumption could be supported by the fact that levels of non-enzymatic antioxidant defenses (NPSH and ascorbic acid) and of a marker of lipid peroxidation (TBARS) did not change significantly

in liver, kidney or testes after acute ZEA administration. Altogether, these results may suggest that ZEA affects enzymatic rather than non-enzymatic markers of oxidative stress, and that increased SOD and CAT activities in fact may counteract SPTLC1 oxidative damage and depletion of non-enzymatic antioxidant defenses. In agreement with our results, Stadnik et al. (2010) have shown increased SOD activity in the liver after 10 days of ZEA (200 and 500 μg/kg, p.o.) administration, and that ascorbic acid content in rat liver was unchanged after 24 h or 10 days of ZEA administration. In addition, catalase activity increased in the liver and kidney of mice 24 h after ZEA (40 mg/kg, i.p.) administration (Zourgui et al., 2008). On the other hand, orally treated male Balb/c mice treatment for 28 days with ZEA (40 mg/kg, i.p.