Vomitoxin Deoxynivalenol

Group B trichothecenes, such as vomitoxin (VT or deoxynivalenol) and similar metabolites 3-acetyl deoxynivalenol and nivalenol, are less toxic than the group A trichothecene T-2 toxin (Bergsj0 et al. 1993). Vomitoxin is produced by Fusarium graminearum and F. culmorum and is a common contaminate of grain used to make human and animal feed. Because it is not destroyed by milling and processing, vomitoxin could be present in human food products at ppm levels (Islam et al. 2003). Swine and other monogastrics are the most sensitive to VT while chickens and turkeys have the highest tolerance to VT (Rotter et al.1996). Ingestion of moderate to low levels can cause anorexia, decreased nutritional efficiency, and immunotox-icity manifest by reduction in natural immunity and poor production performance in food animals. Exposure to high concentrations of VT causes nausea, emesis, leukocyte apoptosis, and circulatory shock (Rotter et al. 1996).

The effects of vomitoxin on immune function have been investigated. In adult mice, levels greater than 0.25 to 0.5 mg/kg/day causes immunotoxicity. A one-time exposure of 10 mg/kg VT caused necrosis of a number of tissues including the bone marrow and lymphoid tissues (Rotter et al. 1996). The effects of VT on cells of the adult immune system may be immunosuppressive or immunostimulatory depending on the length of exposure and dosage.

VT is cytotoxic to a number of cells, including fibroblasts, splenic lymphocytes, and human peripheral blood lymphocytes, because it inhibits protein synthesis at the ribosomal level during the elongation termination step (Rotter et al. 1996). VT at high doses induces rapid apoptotic loss of immature thymocytes and cytotoxic T-lymphocytes in thymus, mature-B lymphocytes in Peyer's patch, and pro/pre B-lymphocytes and mature B-lymphocytes in bone marrow in mice (Bondy and Pestka 2000; Islam et al. 2003). Exposure in the diet to VT at 2 ppm for 5 weeks or 5 ppm for 1 week suppressed mitogenic response of lymphocytes in humans, mice, and chickens (Rotter et al. 1996; Bondy and Pestka 2000). Host resistance to infectious disease is decreased due to a reduction in several cellular functions such as cellmediated immunity, neutrophil migration, and macrophage phagocytosis (Rotter et al. 1996). In contrast to suppression of cellular responses, chronic dietary exposure of VT-induced elevation of serum IgA and increased renal deposition of IgA in mice by cyclooxygenase-2 mediated upregulation of interleukin (IL)-6 (Moon and Pestka 2003). Superinduction of IL-6 is also likely to be responsible for the shock-like and cytotoxic responses with acute high levels of VT exposure (Moon and Pestka 2003). Thus, VT both stimulates and inhibits differing aspects of immune function.

At the present, there are no studies demonstrating VT immunotoxicity in the developing fetus; however, there is evidence that VT is passed on to the egg in chickens, affecting embryo development (Bergsj0 et al. 1993). VT at 1 to 5 mg/kg is not a health hazard to poultry or humans, but in the egg, seriously affected development and hatchability of the chicks. Hens exposed to 0, 2.5, 3, and 5 mg/kg VT in the feed showed no clinical signs of toxicity such as differences in egg production, body weight gain, percentage fertility, or percentage mortality of fertile eggs during incubation (Bergsj0 et al. 1993). However numerous developmental abnormalities were observed in the hatched chicks. Chicks exposed to VT had un-withdrawn yolk sacs, cloacal atresia, delayed ossification of vertebra and extremities, and cardiac malformations (Bergsj0 et al. 1993). This study did not evaluate any immunological parameters in the chicks; however, the tissues targeted by VT exposure included the developing hematopoietic tissues, e.g., yolk sac, bone marrow, and possibly bursa. It is not known if VT is toxic to these developing immune tissues; however, a fair amount of evidence suggests that it may be. VT and T-2 toxin are closely related structurally. Structure activity studies in a number of lymphocyte models suggest that translational arrest is an underlying mechanism for impaired proliferation in both VT and T-2 toxin (Rotter et al. 1996). Both VT and T-2 target immune function and immune tissues, and both induce apoptosis (Bondy and Pestka 2000). These data, although far from indicating that VT is immunotoxic to the developing fetus, show enough similarities between T-2 toxin (a known developmental immunotoxin) and VT that further studies are warranted investigating the developmental immunotoxicity of VT.

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