Interactions between Infections, Nutrients and Xenobiotics

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During recent years there have been several incidents where symptoms of disease have been linked to consumption of food contaminated by chemical substances (e.g. TCDD). Furthermore, outbreaks of infections in food producing animals have attracted major attention with regards to the safety for consumers (e.g., BSE and influenza in chicken). As shown for several xenobiotics in an increasing number of experimental studies, even low-dose xenobiotic exposure may impair immune function over time, as well as microorganism virulence, resulting in more severe infectious diseases and possibly other diseases as well. Also, during ongoing infection, xenobiotic uptake and distribution is often changed resulting in increased toxic insult to the host. The interactions between infectious agents, nutrients, and xenobiotics have thus become a developing concern and new avenue of research in food toxicology, as well as in food-born diseases. From a health perspective, in the risk assessment of xenobiotics in our food and environment, synergistic effects between microorganisms, nutrients, and xenobiotics will have to be considered. Such effects may otherwise gradually change the disease panorama in society. The author of this report is senior food toxicologist at the National Food Administration, Uppsala, Sweden. He is PhD and Adjunct Professor in Experimental Infectious Diseases at the Faculty of Medicine, Uppsala University, Sweden, and a great part of his scientific production has been devoted to the theme covered in this report.



Excretion of Nutrients and Xenobiotics in Infection

The increased uptake of, for example Cd, Ni, and TCDD, in target organs of infection seems to be associated with a more long-term accumulation of these chemical substances in the target organs (Funseth et al., 2000c; Ilback et al., 1992a; Ilback et al., 1992b). One explanation for this association might be that certain potential toxic trace elements compete as well as bind more efficiently and strongly to infection-induced proteins (such as MT) when there is an excess in relation to the physiological concentrations of essential trace elements. In CBV infection a pronounced decrease in As occurs in the target organs of this infection before the inflammatory processes are initiated (Benyamin et al., 2005), whereas Cd in this early phase of disease accumulates in the same organs (Ilback et al., 1992b). Because MT is known to bind both As (Toyama et al., 2002) and Cd (Nordberg and Nordberg, 2000), these results may indicate that Cd competes and has a higher affinity for MT than As. Thus, there seems to exist a competition not only between essential and non-essential trace elements (Goyer, 1997), but also between different non-essential trace elements in infected tissues.


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