Protective effect of Celtis tournefortii against copper-induced toxicity in rat liver

Abstract

This study aimed to investigate the antioxidant and hepatoprotective effects of Celtis tournefortii fruit extract (Ct) against copper-induced liver damage in rats. Thirty-two Wistar Albino rats were divided into four equal groups (n = 8): Control, Copper (Cu), Copper + C. tournefortii (Cu+Ct), and C. tournefortii (Ct). Superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activities, glutathione (GSH) concentration, malondialdehyde (MDA), total antioxidant status (TAS) and total oxidant status (TOS) were analysed in the liver tissues. Liver histopathology was also evaluated. Alanine aminotransferase and lactate dehydrogenase significantly decreased in the Cu+Ct group compared with the Cu group. Oxidative stress parameters MDA and TOS significantly increased with copper administration, whereas they decreased with C. tournefortii co-treatment compared to Cu group. GSH concentration and TAS showed significant decreases with copper administration. Celtis tournefortii co-supplementation with copper significantly enhanced antioxidant parameters such as TAS, SOD, and GPx. Celtis tournefortii remarkably attenuated degenerative and necrotic changes caused by the oral exposure of copper in the liver tissue of rats. Celtis tournefortii may provide amelioration of the antioxidant status and moderation of severity of liver damage against copper toxicity. The therapeutic use of C. tournefortii may exhibit protective effects in liver injury treatment. Antioxidant, hepatoprotective, oriental hackberry, phytochemicals, TAS, TOS Copper (Cu) exposure can occur due to pesticide residue exposure (WHO 2003) in agriculture as well as via drinking water contaminated by environmental pollution or by copper water pipe corrosion (Brewer 2012). Excessive copper intake may also occur via consumption of Cu-rich foods such as liver, seafood, nuts, whole grains, and dried fruits. The tolerable upper intake level is 10 mg/day a value which represents the limit for protection of hepatic injury, a potentially critical side effect of excess copper ingestion (DRI 2001). Cu is a bioelement and a vital transition metal whose deficiency or excess in humans is associated with pathological situations, especially in liver and brain tissues. However, Cu metabolism is generally regulated by absorption and biliary excretion mechanisms. Cu chaperones, Cu transporters, and Cu-binding proteins/enzymes maintain physiological intracellular Cu homeostasis (Pal 2014). On the other hand, excess Cu causes production of free radicals (e.g. reactive oxygen species [ROS]) through Haber-Weiss and Fenton reactions, resulting in tissue damage (Valko et al. 2005). ROS-induced oxidative tissue damage plays an important role in Cu toxicity. For example, excess Cu may lead to peroxidative damage to membrane lipids via the reaction of lipid radicals and oxygen to form peroxy radicals, and causes peroxidation in the membranes of hepatocyte lysosomes. Also, Cu overload also reduces the activity of cytochrome c oxidase and impairs liver mitochondrial respiration (Gaetke et al. 2014). Phytochemicals are bioactive compounds in plants and they exert a protective effect against various diseases (Zhang et al. 2015). Therefore, their nutraceutical use makes them ACTA VET. BRNO 2021, 90: 091–098; https://doi.org/10.2754/avb202190010091 Address for correspondence: Mehmet Ali Temiz Vocational School of Technical Sciences Karamanoğlu Mehmetbey University Karaman, Turkey Phone: +90 338 226 2000 E-mail: [email protected]; [email protected] http://actavet.vfu.cz/