The effect of humic acid in chronic deoxynivalenol intoxication.

The most common mycotoxin found in European foodstuffs, especially unprocessed grains, is deoxynivalenol (DON), which inhibits proteosynthesis and induces oxidative stress. The sorption properties of humic acids (HA) indicate a promising potential in the reduction of mycotoxin intoxication. In an experimental biomodel lasting 35 days, we investigated the effect of a dietary supplement containing HA on the antioxidant status in the liver, heart and kidney mitochondria and in the blood plasma of rats exposed to the stress factor of orally administered DON. DON was administered at doses of 100 and 200% above the maximum tolerable daily intake (1.0 µg/kg body weight/day). We evaluated the activities of the following enzymes: superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione-S-transferase and tripeptide glutathione. Administration of DON has been shown to induce oxidative stress, the intensity of which appears to be directly dependent on the concentration of mycotoxin. Supplementation with 1% HA (10 g/kg of feed) resulted in alleviation of this stress, in which the preventive effect of HA may have been implicated partly by affecting the adsorption of DON through the GIT and limiting its bioavailability. There were also signs that it can act by actively interfering with ROS inhibition to help achieve redox homeostasis. However, there is another aspect that deserves attention, namely, the metabolism of HA. The results presented in our work suggest that the mechanism of possible metabolism occurs predominantly in the liver, including an oxidative increase in polarity and subsequent conjugation reactions mediated by the GST-GSH system.

Effect of humic acids on lead poisoning in bones and on a subcellular level in mitochondria.

Humic acids (HA) are natural substances which exhibit a remarkable spectrum of health benefits, such as their role in chelation. This study aims to supplement the current knowledge on the chelating effects of HA in chronic lead intoxication in rat femurs and in liver, heart and kidney mitochondria in an experiment lasting 10 weeks. Lead acetate trihydrate was administered to rats for 5 weeks at a daily dose of 155.5 mg/kg body weight. At the same time, rats were given three concentrations of HA, with their effect measured over the following 5 weeks. Increased Pb concentrations were detected in the femur after the first week, while HA-administered groups showed a tendency towards inhibiting the increase in Pb deposition. After 5 weeks, Pb concentrations dropped significantly in the HA groups. At the same time, however, other elements were redistributed, with a decrease in Se and Zn being particularly noteworthy. While an increase in Pb concentrations was found after 5 weeks of Pb administration, a concentration of 1% HA resulted in the least significant increase in Pb as well as an increase/decrease in Se/Cu, respectively. In mitochondria, an increase in Pb content was detected after the first and fifth weeks with concomitant redistribution of other elements. At the end of the experiment, again in the 1% HA group, Pb concentrations remained higher only in the liver with the other elements sufficiently normalized, indicating this concentration to be useful in the treatment of Pb intoxication.