Tag Archives: xenobiotics
Disturbance of the transmembrane phosphatidylserine asymmetry in hepatocytes as an apoptosis marker under the action of xenobiotics on rats
O. A. Nakonechna, L. A. Babijchuk, A. I. Bezrodna
Kharkiv National Medical University, Kharkiv, Ukraine;
e-mail: bezrodnaya.ai@gmail.com
It has been reported that unfavorable chemical environmental factors affect the functional state of liver, activate free radical processes against the background of the reduced antioxidant activity, change physico-chemical properties and membrane phospholipid composition of hepatocytes. The aim of our research was to estimate phosphatidylserine distribution in the phospholipid bilayer of hepatocyte membranes and apoptosis stages in hepatocytes of rats under the influence of surfactants: ethyleneglycol (EG), polyethyleneglycol 400, (PEG-400) and polypropyleneglycol (PPG) at a dose of 1/10 DL50. It was found in the subacute toxicological experiment on rats that the investigated xenobiotics EG, PEG-400 and PPG at a dose of 1/10 DL50 caused phosphatidylserine translocation to the outer membrane in the phospholipid bilayer of hepatocytes. This is a specific signal for macrophages aiming at recognition and elimination of apoptotic cells. Analysis of cell death modes under the influence of the investigated xenobiotics at a dose of 1/10 DL50 revealed that the intake of xenobiotics was associated with an increase in the amount of apoptotic/necrotic hepatocytes.
Hepatotoxicity of bisphenol A under conditions of differential supplementation with retinoids
I. O. Shmarakov, V. L. Borschovetska, L. P. Ivanishchuk, M. M. Marchenko
Yuriy Fed’kovych Chernivtsi National University, Ukraine;
e-mail: igor.shmarakov@gmail.com
Classical xenoestrogenic in vivo effects of bisphenol A (2,2-bis(4-hydroxyphenyl)propane, BPA) are well-described in the literature, however the molecular mechanisms of BPA-induced hepatotoxicity are not fully characterized. The work is aimed to assess biochemical markers of BPA induced hepatotoxicity under conditions of differential supplementation with retinoids. We demonstrate that the absence of hepatic retinyl esters as the main form of vitamin A storage provides for a resistance to BPA induced liver damage. Retinoid supplementation increases the hepatotoxic effects of bisphenol A, evidenced in higher indexes of oxidative damage of lipids, proteins and non-protein thiol groups as well as increase of serum alanine aminotransferase activity and myeloperoxidase activity in liver parenchyma. The absence of hepatotoxicity signs when hepatic retinoid stores are depleted and their presence during normal or excessive retinoid supplementation suggest that hepatic retinoid availability is one of the factors determining the hepatotoxicity of bisphenol A.