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.



Metabolism of Nutrients and Xenobiotics in Infection

As described previously, the acute phase reaction during infection results in a down-regulation of the detoxifying system Darnerud et al., 2005; Morgan, 1997) but in an increased synthesis of metal-binding proteins important for host defence. Two such proteins are ceruloplasmin (a Cucontaining protein) (Friman et al., 1982; Ilback et al., 1983) and MT (Funseth et al., 2002a; Ilbäck et al 2004a). During early CBV infection, (Ilback et al., 1983) the amount of MT increases about five-fold in the liver and kidneys (Funseth et al., 2002a; Ilback et al., 2004a). This induction of MT, even at normal physiological levels of trace elements, results in redistribution of Cd and Cu from the liver to the kidneys (Ilback et al., 2004a). Influenza infection has also been shown to induce gene expression of MT in both the liver and the lungs (Ghoshal et al., 2001). With increased capacity of binding, MT can bind Zn, Cd, Hg, and Cu (Nordberg and Nordberg, 2000), but interactions with other metals cannot be excluded when these are present in large quantities or when there is a shortage of essential trace elements (Goyer, 1997). The infectionassociated induction of metal-binding proteins can account for an altered trace element balance in infected organs and a prolonged persistent accumulation of chemicals in target organs of infection that may affect the growth and virulence of microorganisms, as well as repair processes in inflammatory tissue lesions.


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