Effects of carnosine on apoptosis, TRPM2 ion channels, and betatrophin hormone in kidney and liver tissues of rats experimentally exposed to formaldehyde

Formaldehyde (FA) causes oxidative stress in the tissues and deteriorates the energy metabolism. We assumed in our study that the known adverse effects of FA on kidneys and liver might be related to the increase of the activation in the transient receptor potential melastatin 2 (TRPM2) channels, which could be activated with the oxidative stress from the ion channels in the cellular membranes. Likewise, we suggested that there could be a correlation between the FA, which could deteriorate the energy metabolism, and the betatrophin, a lipid metabolism regulator. Moreover, we aimed to demonstrate whether the known beneficial effect of carnosine (an antioxidant agent) on the liver damage caused by FA is also acceptable for kidneys and the correlation of the TRPM2 channels and betatrophin with the possible healing effect of the carnosine in both tissues. In our study, we used 28 male rats (Sprague Dawley) between weeks 8 and 10 and with an average weight of 260 grams. The betatrophin levels in the blood, kidney and liver tissue supernatants were analyzed with ELISA method, and the total oxidant levels (TOL) and total antioxidant levels (TAL) were analyzed with the Rel Assay. The betatrophin and TRPM2 immunoreactivity in the renal and hepatic tissues was determined with the immunohistochemical method. In addition, we used TUNEL method for the determination of the apoptotic cells. FA exposure caused severe damage to the renal and hepatic tissues. In addition, while FA exposure decreased the betatrophin concentrations in the renal and hepatic tissues and blood, increased the TO levels, decreased the TA levels and increased the TUNEL positivity, it also activated the TRPM2 channels. Carnosine supplementation improved significantly the histopathological and biochemical changes caused by FA. In conclusion, carnosine, which was administered for the treatment of the oxidative damage caused by the FA exposure, suppressed the oxidative stress and thus improved this damage almost completely.