This study investigated the kynurenine metabolism in rats treated with cadmium. We used an animal model at the levels of Cd corresponding to human environmental and occupational exposure to this metal which allows the assessment of its early effect on the structure and function of kidneys. We observed significant decrease in the serum concentration of tryptophan (TRP) and its metabolites: kynurenine (KYN), kynurenic acid (KYNA), and 3-hydroxykynurenine (3-HKYN), which was accompanied by a decrease in KYN derivatives in kidney and liver tissues. This effect was dependent on the level of Cd exposure. Regression analysis showed negative correlations between blood concentrations of Cd and TRP derivatives in serum, kidney and liver tissues.
Conversely, the urinary concentration of KYN and KYNA increased. Changes in product degradation of TRP after Cd treatment were proportional to the severity of renal damage and correlated with the concentration of proximal tubular injury marker - urinary isoenzyme B of N-acetyl-D-glucosaminidase (NAG-B).
Our results seem to indicate that intoxication with Cd induced significant disturbances in the peripheral kynurenine pathway.