Apoptosis and regeneration of hepatocytes in rats orally exposed to caffeinated energy drinks

• Published in: Comparative clinical pathology 2020-04, Vol.29 (2), p.477-483
• Main Authors: Gubina-Vakulyck, Galina, Gorbach, Tatiana, Onishchenko, Anatolii, Novikova, Viktoriia, Nakonechna, Oksana, Tryfonova, Nataliia, Butova, Tetiana, Tkachenko, Anton
• Format: Article
• Language: English
• Subjects: Alanine; Alanine transaminase; Apoptosis; Aspartate aminotransferase; Beverages; Body weight; Caffeine; Caspase-3; Cell death; Chromatin; Cytolysis; Drinking water; Energy drinks; Hematology; Hepatocytes; Liver; Medicine; Medicine & Public Health; Oncology; Original Article; Parenchyma; Pathology; Poly(ADP-ribose) polymerase; Ribose; Statistical analysis
• ISSN: 1618-5641; 1618-565X
• DOI: 10.1007/s00580-019-03079-7

Caffeinated energy drinks (CEDs) have become extremely popular over the last decade. In recent years, many researchers have raised a concern about the safety of CEDs. The aim of our study was to evaluate the morphology of the liver, as well as the features of hepatocyte apoptosis/regeneration, in rats orally exposed to CEDs for 2 weeks. Sixteen WAG rats formed two equal groups. Rats from the experimental group were orally exposed to a CED at a dose of 12 ml/kg of body weight for 2 weeks. The control group consisted of intact animals with the provided access to drinking water instead. The content of apoptosis marker caspase-3 and the activity of poly-(ADP-ribose) polymerase (PARP) were evaluated in liver homogenates. The activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) was determined in the blood serum. Hepatic Ki-67 expression was quantitatively assessed immunohistochemically. A statistically significant increase in the level of caspase-3 and a decrease in the activity of PARP in liver homogenates against the background of energy drink consumption by rats indicate the activation of hepatocyte apoptosis, evidenced by chromatin margination of hepatocytes as well. Cytolysis of hepatocytes was confirmed by the elevation of ALT and AST. In response to cell death, liver parenchyma starts proliferating. This fact is supported by the statistically significant increase in the amount of Ki-67 + hepatocytes in rats exposed to CED compared with controls. Oral exposure to a CED during 2 weeks promotes liver damage, apoptosis, and regeneration of hepatocytes.