Potential genotoxic, apoptotic, inflammatory and biochemical effects of long-term propofol anaesthesia in rabbit tissues

Propofol, that is metabolised by the brain, kidneys, and liver, is one of the most preferred intravenous sedative-hypnotic agents. Although it has antioxidant effects during short-term use, it triggers the occurrence of oxidative stress during long-term use. Propofol causes disruption of tissue integrity through its apoptotic, necrotic, and genotoxic effects. Studies in the literature are primarily conducted on acute administration and/or a single tissue. Thus, the information pool regarding the impacts of long-term propofol exposure on different tissue types is quite limited. Therefore, to identify its genotoxic, apoptotic, inflammatory, and biochemical effects in these tissues of Oryctolagus cuniculus following 6-, 12-, and 24-hour propofol administration, DNA damage, activities of Caspase and antioxidant enzymes, concentrations of inflammatory necrosis signalling proteins and total proteins were measured. In addition, to reveal variations and relations of these parameters in each tissue, principal component and multivariate correlation analyses were used. Considering the results, it was determined that in the kidney, genotoxicity, apoptosis, and inflammation increased the most in relation to the cumulative propofol administration, whereas in the liver there was a lesser change in DNA and tissue damage. It was observed that propofol administration significantly increased oxidative stress responses in brain tissues. In the liver, administration for 6hours triggered antioxidant enzyme activities, while activations gradually decreased at the 12- and 24-hour points. Thus, it was concluded that chronic propofol administration can cause greater damage to the brain and kidneys than to the liver, and that adverse effects increase in parallel with prolonged administration.