%0 Journal Article
%T Effects of Propofol, a Sedative-Hypnotic Drug, on the Lipid Profile, Antioxidant Indices, and Cardiovascular Marker Enzymes in Wistar Rats
%A Oluwatosin A. Adaramoye
%A Olugbenga Akinwonmi
%A Olubukola Akanni
%J ISRN Pharmacology
%D 2013
%R 10.1155/2013/230261
%X In recent years, the activity of anaesthetic propofol on biological processes has been attracting attention. The effect of propofol on biochemical indices in animals is unknown. In this study, we examined the effects of propofol on lipid profile, antioxidant indices, and cardiovascular marker (CVM) enzymes in rats. The study consists of three groups of seven rats each. Group one received corn oil (Control) while groups two and three received propofol (doses of 2 and 4£¿mg/kg body weight, resp.). Results showed that administration of propofol caused a significant ( ) and dose-dependent increase in the levels of total bilirubin. Propofol at 2 and 4£¿mg/kg increased the levels of serum total cholesterol by 74% and 55%, triglycerides by 97% and 115%, and LDL-C (low-density lipoprotein-cholesterol) by 45% and 73%, respectively, while HDL-C (high-density lipoprotein-cholesterol) decreased by 41% and 54%, respectively. Propofol significantly ( ) increased the levels of the hepatic reduced glutathione (GSH) and activities of GSH-dependent enzymes. Propofol at 2 and 4£¿mg/kg increased the activities of CVM enzymes: lactate dehydrogenase by 1.7 and 1.8 folds and creatinine phosphokinase by 2.0 and 2.1 folds, respectively. Taken together, propofol increased the levels of GSH and GSH-dependent enzymes but adversely affected the lipid profile of the rats. 1. Introduction Oxidative stress can be described as an imbalance between the production of free radicals and antioxidant defence. Over the last decades, it has become amply evident that oxidative stress, usually in the form of reactive oxygen species (ROS), is a critical pathogenic factor in the development of several systemic diseases [1, 2]. Therefore, inhibition of ROS formation, scavenging of ROS, or interfering with ROS pathogenic signaling pathways might be the potential ways to protect against oxidative stress-induced ailments [3]. Propofol (2,6-diisopropylphenol) (Figure 1), a highly lipid-soluble anaesthetic, is widely used for induction and maintenance of general anaesthesia. Propofol ameliorates oxidative injury in several organs, including the heart [4], lungs [5], brain [6], liver [7], and testis [8]. Propofol is chemically similar to the endogenous antioxidant ¦Á-tocopherol (vitamin E) and, theoretically, it should have similar properties [9]. It is not surprising therefore that many studies have demonstrated antioxidant effects of propofol in vitro [10¨C12] and in vivo [13]. Propofol has also been shown to elicit antiapoptotic effect in human umbilical vein endothelial cells by acting as an antioxidant
%U http://www.hindawi.com/journals/isrn.pharmacology/2013/230261/