Various healing effects of peat therapy were attributed to the anti-inflammatory activity of (Humic Substances). Taugner (1963) showed in the rat paw edema model that sodium humate significantly inhibits the development of various edemas compared with untreated controls.
As found by Klocking et al. (1968) in the same model, ammonium humate isolated from peat water exceeds the anti-inflammatory effect of sodium humate and is twice as effective as acetylsalicylic acid (aspirin) and amino-phenazone, respectively. Amosova et al. (1990), in evaluating the biologic activity of HA from Tambukan therapeutic mud in animals, found (Humic Acid) (10 mg/kg) to suppress both phases of the inflammatory process: the exudation (by 44 %) and the proliferation process (by 50-55%).
The anti-inflammatory effect of (Humic Substances) has been supported by a plausible biochemical explanation. As demonstrated by Schewe et al. (1991), naturally occurring (Humic Acid), and even more synthetic (Humic Acid)-like polymers, inhibit the lipoxygenase pathway of the arachidonic acid (AA) cascade. AA is an integral part of the cell membrane, and the substrate for the synthesis of eicosanoid-based inflammation mediators such as leukotrienes, thromboxane and prostacyclin.
Recently, (Humic Acid) (sodium humate) as well as various synthetic HA-like polymers were also found to suppress the heat-induced (42 8C, 6 h) AA release of human pro-monocytic U937cells (Dunkelberg et al., 1997; Klocking et al., 1997). The inhibition of AA release was most pronounced in cells treated with nontoxic concentrations (20 mg/mL) of 3,4-DHPOP (96%) and 3,4-DHTOP (92%), respectively (Table 3). CHOP, sodium humate, KOP and BOP protected cells from membrane damage at 65 ± 90%. These findings may be indicative for membrane-protective activities of (Humic Acid) type substances.
Unlike 5-lipoxygenase, phospholipase A (porcine pancreas), the rate-limiting key enzyme of the AA cascade, is strongly activated at low (Humic Acid) concentrations (0.1 ± 1 mg/mL) and normalized or slightly inhibited at high (Humic Acid) concentrations (Klocking et al., 1999). The shape of the dose-response curve suggests (Humic Substances) to have a regulatory function on PLA activity.
In referring to the function of (Humic Substances) as electron donor-acceptor system, Jurcsik (1994) discussed the behavior of (Humic Substances) as the consequence of a `buffering effect'; this means that (Humic Acids) are able to produce as well as to bind activated oxygen species. This regulatory system is assumed to be important for the favorable influence of (Humic Substances) on wound healing and killing of cancer cells (Jurcsik, 1994).
