Aldehydes participation in oxidative stress in rat thymocytes in vitro

A variety of lipid radicals are formed under oxidative stress development. The further oxidation of these radicals leads to formation of numerous aldehydes. They can form postsynthetic modifications in proteins and nucleic acids that disrupt their functions. In the present study aldehydes role in the formation of oxidative stress parameters in rat thymocytes was investigated. Two models were used: iron-stimulated oxidative stress and exogenous aldehydes exposure to thymocytes. For oxidative stress induction, thymocytes (2 x 10(6) cells/ml HBSS, pH 7.2) were exposed to different concentrations of FeSO4 (20, 30, 40 microM) and ascorbic acid (100 microM) for 6 h. It resulted in increase of levels of aldehydes 29 times (90 +/- 6 nmol/10(7) cells), these changes led to increase of TBARS levels 4.4 times; the levels of protein CO groups 10 times, cell mitochondrial activity and low-molecular weight SH groups were decreased 1.5 and 2.3 times, respectively. Treatment with aldehydes acceptor dimedone (200 microM) significantly decreased the levels of aldehydes 3.7 times, TBARS 1.6 times and protein CO groups 5 times. It was shown that the levels of cell mitochondrial activity increase 1.4 times and the levels of SH groups 1.8 times. To compare the effects of aldehydes in induction of oxidative stress, thymocytes (2 x 10(6) cells/ml HBSS, pH 7.2) were exposed to 50-600 microM formaldehyde (FA), 50-600 microM glyoxal (GL), 50-600 microM methylglyoxal (MGL), 1-15 microM acrolein (ACR) for 6 h. TBARS levels were increased for FA 1.3 times and for other aldehydes about 5-7 times. The levels of protein CO groups were increase for FA 3.7 times, for MGL 7 times, for GL 13 times, for ACR 22 times. Levels of SH groups were decreased for FA 1.5 times, for MGL 2.6 times, for GL 3 times, for ACR 9 times. A decrease of cell mitochondrial activity 1.5 times observe for all aldehydes. Obtained results prove the aldehydes participation in the formation of oxidative stress parameters and their capability to oxidative stress induction in the rat thymocytes.